539 results on '"Pariente, Jérémie"'
Search Results
202. Additional file 2: of Case report of Lewy body disease mimicking Creutzfeldt-Jakob disease in a 44-year-old man
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Saint-Aubert, Laure, Pariente, Jérémie, Herve Dumas, Payoux, Pierre, Jean-Philippe Brandel, Puel, Michèle, Vital, Anne, Guedj, Eric, Lesage, Suzanne, Peoc’h, Katell, Courbon, Christine Brefel, and Magne, Fabienne Ory
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3. Good health - Abstract
Imaging regional quantification. The table displays z-scores from quantitative comparison of 18F-FDG uptake and grey matter density between the patient and age-matched control groups. (DOC 92 kb)
203. Additional file 2: of Case report of Lewy body disease mimicking Creutzfeldt-Jakob disease in a 44-year-old man
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Saint-Aubert, Laure, Pariente, Jérémie, Herve Dumas, Payoux, Pierre, Jean-Philippe Brandel, Puel, Michèle, Vital, Anne, Guedj, Eric, Lesage, Suzanne, Peoc’h, Katell, Courbon, Christine Brefel, and Magne, Fabienne Ory
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3. Good health - Abstract
Imaging regional quantification. The table displays z-scores from quantitative comparison of 18F-FDG uptake and grey matter density between the patient and age-matched control groups. (DOC 92 kb)
204. Cerebral representation of a sensory discrimination network in humans
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Chollet, François, Dobkin, Bruce, Pariente, Jeremie, Saab, Fred, Cohen, Mark, Loubinoux, Isabelle, and Mazziotta, John
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- 2000
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205. Clinical Effect of Early vs Late Amyloid Positron Emission Tomography in Memory Clinic Patients
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Altomare, Daniele, Barkhof, Frederik, Caprioglio, Camilla, Collij, Lyduine E., Scheltens, Philip, Lopes Alves, Isadora, Bouwman, Femke, Berkhof, Johannes, van Maurik, Ingrid S., Garibotto, Valentina, Moro, Christian, Delrieu, Julien, Payoux, Pierre, Saint-Aubert, Laure, Hitzel, Anne, Molinuevo, José Luis, Grau-Rivera, Oriol, Gispert, Juan Domingo, Drzezga, Alexander, Jessen, Frank, Zeyen, Philip, Nordberg, Agneta, Savitcheva, Irina, Jelic, Vesna, Walker, Zuzana, Edison, Paul, Demonet, Jean-François, Gismondi, Rossella, Farrar, Gill, Stephens, Andrew W., Frisoni, Giovanni B., Abdelnour, Carla, Aguilera, Nuria, Aksman, Leon, Alarcón-Martín, Emilio, Alegret, Montse, Alonso-Lana, Silvia, Andersen, Pia, Arab, Majd, Aspö, Malin, Bader, Ilona, Bader, Ilse, Banton, Nigel, Barnes, Rodrigo, Barrie, Dawn, Battle, Mark, Belén Collado, Ana, Bellet, Julie, Biger, Marine, Birck, Cindy, Bischof, Gerard, Boada, Mercè, Boellaard, Ronald, Bogdanovic, Nenad, Bollack, Ariane, Bombois, Stéphanie, Borg, Stefan, Borjesson-Hanson, Anne, Boskov, Vladimir, Boutantin, Justine, Boutoleau-Bretonniere, Claire, Breuilh, Laetitia, Bringman, Eva, Brunel, Baptiste, Bucci, Marco, Buckley, Chris, Buendía, Mar, Bullich, Santi, Calvet, Anna, Cañada, Laia, Cañada, Marta, Cardoso, Jorge, Carlier, Jasmine, Carre, Elise, Carrie, Isabelle, Cassagnaud, Pascaline, Cassol, Emmanuelle, Castilla-Martí, Miguel, Cazalon, Elodie, Chaarriau, Tiphaine, Chaigeau, Rachel, Chalmers, Taylor, Clerc, Marie-Thérèse, Clerigue, Montserrat, Cognat, Emmanuel, Coll, Nina, Connely, Peter, Cordier, Elodie, Costes, Corine, Coulange, Camille, Courtemanche, Hélène, Creisson, Eric, Crinquette, Charlotte, Cuevas, Rosario, Cufi, Marie-Noëlle, Dardenne, Sophie, de Arriba, Maria, de Costa Luis, Casper, de Gier, Yvonne, de Verbizier Lonjon, Delphine, Dekker, Veronique, Dekyndt, Bérengère, Delbeuck, Xavier, Deramecourt, Vincent, Desclaux, Françoise, Diaz, Carlos, Diego, Susana, Djafar, Mehdi, Dölle, Britta, Doull, Laura, Dricot, Laurence, Dubois, Bruno, Dumont, Julien, Dumur, Jean, Dumurgier, Julien, Dvorak, Martin, Ecay, Mirian, Escher, Claus, Estanga, Ainara, Esteban, Ester, Fanjaud, Guy, Fauria, Karine, Felez Sanchez, Marta, Feukam Talla, Patrick, Ford, Lisa, Fuster, David, Gabelle, Audrey, Gaubert, Sinead, Gauci, Cédric, Geldhof, Christine, Georges, Jean, Ghika, Joseph, González, Elena, Goovaerts, Valerie, Goulart, Denis Mariano, Grasselli, Caroline, Gray, Katherine, Greensmith, Martin, Grozn, Laure, Guillemaud, Céline, Gunn, Fiona, Guntur Ramkumar, Prasad, Hagman, Göran, Hansseuw, Bernard, Heeman, Fiona, Hendriks, Janine, Himmelmann, Jakob, Hives, Florent, Hoenig, Merle, Hourrègue, Claire, Hudson, Justine, Huguet, Jordi, Ibarria, Marta, Iidow, Ifrah, Indart, Sandrine, Ingala, Silvia, Ivanoiu, Adrian, Jacquemont, Charlotte, Jiao, Jieqing, Jofresa, Sara, Jonsson, Cathrine, Kaliukhovich, Dzmitry, Kern, Silke, Kivipelto, Miia, Knezevic, Iva, Kuchcinski, Grégory, Laforce, Manon, Lafuente, Asunción, Lala, Françoise, Lammertsma, Adriaan, Lax, Michelle, Lebouvier, Thibaud, Lee, Ho-Yun, Lee, Lean, Leeuwis, Annebet, Lefort, Amandine, Legrand, Jean-François, Leroy, Mélanie, Lesoil Markowski, Constance, Levy, Marcel, Lhommel , Renaud, Lopes, Renaud, Lorenzini, Luigi, Lorette, Adrien, Luckett, Emma, Lundin, Marie, Mackowiak, Marie-Anne, Malotaux, Vincent, Manber, Richard, Manyakov, Nikolay, Markiewicz, Pawel, Marne, Paula, Marquié, Marta, Martín, Elvira, Martínez, Joan, Martinez Lage, Pablo, Mastenbroek, Sophie E., Maureille, Aurélien, Meersmans, Karen, Mett, Anja, Milne, Joseph, Minguillón, Carolina, Modat, Marc, Montrreal, Laura, Müller, Theresa, Muniz, Graciela, Mutsarts, Henk Jan, Nilsson, Ted, Ninerola, Aida, Novaes, Wilse, Nuno Carmelo Pires Silva, Joao, Operto, Greg, Orellana, Adela, Ousset, Pierre-Jean, Outteryck, Olivier, Pallardy, Amandine, Palombit, Alessandro, Pancho, Ana, Pappon, Martin, Paquet, Claire, Pariente, Jérémie, Pasquier, Florence, Peaker, Harry, Pelejà, Esther, Pennetier, Delphine, Pérez-Cordón, Alba, Perissinotti, Andrés, Perrenoud, Matthieu Paul, Petit, Sandrine, Petyt, Grégory, Pfeil, Julia, Pirotte, Blanche, Pla, Sandra, Plaza Wuthrich, Sonia, Poitrine, Lea, Pollet, Marianne, Poncelet, Jean-Benoit, Prior, John, Pruvo, Jean-Pierre, Putallaz, Pauline, Queneau, Mathieu, Quenon , Lisa, Rădoi, Andreea, Rafiq, Marie, Ramage, Fiona, Ramis, Maribel, Reinwald, Michael, Rios, Gonzalo, Ritchie, Craig, Rodriguez, Elena, Rollin, Adeline, Rouaud, Olivier, Sacuiu, Simona, Sala, Arianna, Salabert, Anne-Sophie, Saldias, Jon, Salvadó, Gemma, Sanabria, Angela, Sannemann, Lena, Sastre, Nathalie, Savina, Daniela, Schaeverbeke, Jolien, Schildermans, Carine, Schmidt, Mark, Schöll, Michael, Schuermans, Jeroen, Semah, Franck, Shekari, Mahnaz, Skoog, Ingmar, Sotolongo-Grau, Oscar, Stephens, Andrew, Stewart, Tiffany, Stutzmann, Jennyfer, Tait, Murray, Tárraga, Lluis, Tartari, Juan Pablo, Tysen-backstrom, Ann-christine, Valero, Sergi, Vallez Garcia, David, van Berckel, Bart N.M., van Essen, Martijn, Van Laere, Koen, van Leur, Jeroen, Vandenberghe, Rik, Vellas, Bruno, Virolinen, Jukka, Visser, Pieter Jelle, Walles, Håkan, Wallin, Emilia, Whitelaw, Grant, Wimberley, Catriona, Win , Zarni, Wink, Alle Meije, Wolz, Robin, Woodside, John, Yaqub, Maqsood, and Zettergren, Anna
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206. Huntington's Disease with Small CAG Repeat Expansions.
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Heinzmann, Anna, Sayah, Sabrina, Lejeune, François‐Xavier, Hahn, Valérie, Teichmann, Marc, Monin, Marie‐Lorraine, Marchionni, Enrica, Gérard, Fleur, Charles, Perrine, Pariente, Jérémie, and Durr, Alexandra
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Background: Carriers of small cytosine‐adenine‐guanine (CAG) repeats below 39 in the HTT gene are traditionally associated with milder Huntington's disease, but their clinical profile has not been extensively studied. Objective: To study the phenotype of CAG36‐38 repeat carriers. Methods: We included 35 patients and premanifest carriers of CAG36‐38 repeats. We compared clinical and neuropsychological profiles of 11 CAG36‐38 patients with 11 matched CAG40‐42 patients. In addition, we analyzed 243 CAG36‐38 individuals from the ENROLL study to complete the phenotype description. Results: Global cognitive efficiency and performance in different cognitive subdomains were similar in small CAG36‐38 and typically CAG40‐42 expanded individuals. Chorea as the first symptom was significantly less frequent for CAG36‐38 patients (P = 0.04) despite similar total motor scores at first visit. Total motor score at last visit was significantly lower in CAG36‐38 carriers (P = 0.003). The similar cognitive and different motor profile of CAG36‐38 (n = 243) and CAG40‐42 (n = 4675) carriers was confirmed in the ENROLL database. Additionally, clinicians were significantly less confident in diagnosing Huntington's disease (P = 2.4e−8) and diagnosis happened significantly later in CAG36‐38 (P = 2.2e−6) despite a similar age at symptom onset (P = 0.29). Conclusions: We showed that small CAG36‐38 expansion carriers had a similar cognitive profile to those with the more common CAG40‐42 expansions. These individuals may evade molecular diagnosis because of the absence of chorea rather than because of a low penetrance of symptoms. This finding should encourage neurologists to consider Huntington's disease in cognitively impaired elderly patients without typical chorea and anticipate consequences for genetic counseling in their offspring. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]
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- 2023
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207. Can neurodevelopmental disorders influence the course of neurodegenerative diseases? A scoping review.
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Siguier, Perrine L.M., Planton, Mélanie, Baudou, Eloise, Chaix, Yves, Delage, Alix, Rafiq, Marie, Wolfrum, Marie, Gérard, Fleur, Jucla, Mélanie, and Pariente, Jérémie
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NEURODEGENERATION , *ALZHEIMER'S disease , *DISEASE progression , *LEARNING disabilities , *DISEASE risk factors - Abstract
This scoping review aims at giving an overview of the possible influence of neurodevelopmental disorders (NDDs) on cognitive-behavioral neurodegenerative diseases (CBNDs). Based on the PRISMA-ScR checklist, it details the methods of NDDs screening, the identified NDDs-CBNDs associations, as well as the criteria and types of association. The last literature search was performed in June 2023. In the final study, 32 articles were included. Analysis first showed that NDDs were mainly detected through medical records screening. Second, the association of specific learning disorders and major or mild neurocognitive disorder due to Alzheimer's disease was the most investigated. Third, associations were mostly based on prevalence comparisons. Finally, 66 % of studies reported a positive association between NDDs and CBNDs. Notably, up to 67 % of positive associations were observed with atypical forms of certain CBNDs. Authors' interpretations suggest that NDDs could constitute a risk factor for CBNDs. However, the influence of NDDs on CBNDs still lacks evidence and biological support, possibly due to the heterogeneity of methods and criteria employed. Developing validated assessment tools for all NDDs and conducting cohort studies could be beneficial for research, and clinical practice. Indeed, this review also underlines the importance of adopting a life-span approach regarding CBNDs. • NDDs may be a risk factor for dementia, especially for atypical variants. • The biological and temporal processes involved remain hypothetical. • A lifespan approach should be adopted in both clinical practice and research. • This lifespan approach requires methodological breakthroughs. [ABSTRACT FROM AUTHOR]
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- 2024
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208. Exploring the impact of the interthalamic adhesion on human cognition: insights from healthy subjects and thalamic stroke patients.
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Vidal, Julie P., Rachita, Kévin, Servais, Anaïs, Péran, Patrice, Pariente, Jérémie, Bonneville, Fabrice, Albucher, Jean-François, Danet, Lola, and Barbeau, Emmanuel J.
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STROKE patients , *COGNITION , *NEUROPSYCHOLOGICAL tests , *STROKE , *COGNITION disorders - Abstract
The interthalamic adhesion (IA) is a structure that connects the median borders of both thalami. Its anatomical variants and functions remain poorly studied. The main objective of this study was to explore the role of the IA on cognition. 42 healthy subjects and 40 patients with chronic isolated thalamic strokes underwent a neuroimaging and a neuropsychological assessment. The presence, absence, or lesion of the IA and its anatomical variants were evaluated. 76% of participants had an IA, with a higher prevalence among women (92%) than men (61%). The presence or absence of an IA did not affect the neuropsychological performance of healthy subjects nor did the type of IA variant. Across all the tests and when compared to healthy subjects using a Bayesian rmANOVA, patients exhibiting more cognitive impairments were those
without an IA (n = 10, BF10 = 10,648), while thosewith an IA were more preserved (n = 18, BF10 = 157). More specifically, patientswithout an IA performed more poorly in verbal memory or the Stroop task versus healthy subjects. This was not explained by age, laterality of the infarct, volume or localization of the lesion. Patientswith a lesioned IA (n = 12) presented a similar trend to patientswithout an IA, which could however be explained by a greater volume of lesions. The IA does not appear to play a major role in cognition in healthy subjects, but could play a compensatory role in patients with thalamic lesions. [ABSTRACT FROM AUTHOR]- Published
- 2024
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209. Prevalence and characteristics of vascular cognitive impairment in a European cohort of adult patients with Moyamoya angiopathy.
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Giroud, Marine, Calviere, Lionel, Machado, Carla, Reyes, Sonia, Mirabel, Hélène, Raposo, Nicolas, Brandicourt, Pierre, Viguier, Alain, Albucher, Jean-François, Bonneville, Fabrice, Olivot, Jean Marc, Péran, Patrice, Pariente, Jérémie, Hervé, Dominique, and Planton, Mélanie
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COGNITIVE processing speed , *EXECUTIVE function , *COGNITION disorders , *ADULTS , *MAGNETIC resonance imaging - Abstract
Introduction: Moyamoya angiopathy (MMA) is associated with a high risk of stroke, but it is also increasingly recognized as leading to cognitive impairment. The aim of this study was to determine the prevalence, nature, and severity of vascular cognitive impairment no dementia (VCIND) in adults with MMA and to identify clinical and imaging factors associated with VCIND.We conducted a retrospective study of consecutive adult patients with MMA followed in two tertiary hospitals (Toulouse and Paris Lariboisiere). All patients underwent neuropsychological assessment and brain magnetic resonance imaging (MRI). VCIND was defined as at least two variables of the same cognitive process with z-scores of < 2 standard deviations, regardless of the cognitive domain, that do not interfere in everyday life. Baseline demographic, clinical, and imaging data were compared between patients with and without VCIND.A total of 102 patients (mean age 43 years; 65% women) were included. Thirty-four patients (33.3%) had VCIND. VCIND was mild in 20/34 (59%), moderate in 8/34 (23%), and severe in 6/34 (18%) patients. Executive function was the most widely affected (25.5%), followed by attention and processing speed (24.8%). In univariable analyses, VCIND was associated with ischemic stroke at diagnosis and the presence of ischemic lesions on MRI.VCIND is highly prevalent in adults with MMA. Executive functions and processing speed are predominantly affected. These findings may guide clinicians in their evaluation of patients with MMA. Further research should assess the effect of revascularization therapies on cognitive functions.Methods: Moyamoya angiopathy (MMA) is associated with a high risk of stroke, but it is also increasingly recognized as leading to cognitive impairment. The aim of this study was to determine the prevalence, nature, and severity of vascular cognitive impairment no dementia (VCIND) in adults with MMA and to identify clinical and imaging factors associated with VCIND.We conducted a retrospective study of consecutive adult patients with MMA followed in two tertiary hospitals (Toulouse and Paris Lariboisiere). All patients underwent neuropsychological assessment and brain magnetic resonance imaging (MRI). VCIND was defined as at least two variables of the same cognitive process with z-scores of < 2 standard deviations, regardless of the cognitive domain, that do not interfere in everyday life. Baseline demographic, clinical, and imaging data were compared between patients with and without VCIND.A total of 102 patients (mean age 43 years; 65% women) were included. Thirty-four patients (33.3%) had VCIND. VCIND was mild in 20/34 (59%), moderate in 8/34 (23%), and severe in 6/34 (18%) patients. Executive function was the most widely affected (25.5%), followed by attention and processing speed (24.8%). In univariable analyses, VCIND was associated with ischemic stroke at diagnosis and the presence of ischemic lesions on MRI.VCIND is highly prevalent in adults with MMA. Executive functions and processing speed are predominantly affected. These findings may guide clinicians in their evaluation of patients with MMA. Further research should assess the effect of revascularization therapies on cognitive functions.Results: Moyamoya angiopathy (MMA) is associated with a high risk of stroke, but it is also increasingly recognized as leading to cognitive impairment. The aim of this study was to determine the prevalence, nature, and severity of vascular cognitive impairment no dementia (VCIND) in adults with MMA and to identify clinical and imaging factors associated with VCIND.We conducted a retrospective study of consecutive adult patients with MMA followed in two tertiary hospitals (Toulouse and Paris Lariboisiere). All patients underwent neuropsychological assessment and brain magnetic resonance imaging (MRI). VCIND was defined as at least two variables of the same cognitive process with z-scores of < 2 standard deviations, regardless of the cognitive domain, that do not interfere in everyday life. Baseline demographic, clinical, and imaging data were compared between patients with and without VCIND.A total of 102 patients (mean age 43 years; 65% women) were included. Thirty-four patients (33.3%) had VCIND. VCIND was mild in 20/34 (59%), moderate in 8/34 (23%), and severe in 6/34 (18%) patients. Executive function was the most widely affected (25.5%), followed by attention and processing speed (24.8%). In univariable analyses, VCIND was associated with ischemic stroke at diagnosis and the presence of ischemic lesions on MRI.VCIND is highly prevalent in adults with MMA. Executive functions and processing speed are predominantly affected. These findings may guide clinicians in their evaluation of patients with MMA. Further research should assess the effect of revascularization therapies on cognitive functions.Conclusions: Moyamoya angiopathy (MMA) is associated with a high risk of stroke, but it is also increasingly recognized as leading to cognitive impairment. The aim of this study was to determine the prevalence, nature, and severity of vascular cognitive impairment no dementia (VCIND) in adults with MMA and to identify clinical and imaging factors associated with VCIND.We conducted a retrospective study of consecutive adult patients with MMA followed in two tertiary hospitals (Toulouse and Paris Lariboisiere). All patients underwent neuropsychological assessment and brain magnetic resonance imaging (MRI). VCIND was defined as at least two variables of the same cognitive process with z-scores of < 2 standard deviations, regardless of the cognitive domain, that do not interfere in everyday life. Baseline demographic, clinical, and imaging data were compared between patients with and without VCIND.A total of 102 patients (mean age 43 years; 65% women) were included. Thirty-four patients (33.3%) had VCIND. VCIND was mild in 20/34 (59%), moderate in 8/34 (23%), and severe in 6/34 (18%) patients. Executive function was the most widely affected (25.5%), followed by attention and processing speed (24.8%). In univariable analyses, VCIND was associated with ischemic stroke at diagnosis and the presence of ischemic lesions on MRI.VCIND is highly prevalent in adults with MMA. Executive functions and processing speed are predominantly affected. These findings may guide clinicians in their evaluation of patients with MMA. Further research should assess the effect of revascularization therapies on cognitive functions. [ABSTRACT FROM AUTHOR]
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- 2024
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210. Explaining the association between social and lifestyle factors and cognitive functions: a pathway analysis in the Memento cohort.
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Grasset, Leslie, Proust-Lima, Cécile, Mangin, Jean-François, Habert, Marie-Odile, Dubois, Bruno, Paquet, Claire, Hanon, Olivier, Gabelle, Audrey, Ceccaldi, Mathieu, Annweiler, Cédric, David, Renaud, Jonveaux, Therese, Belin, Catherine, Julian, Adrien, Rouch-Leroyer, Isabelle, Pariente, Jérémie, Locatelli, Maxime, Chupin, Marie, Chêne, Geneviève, and Dufouil, Carole
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COGNITIVE ability , *SOCIAL factors , *STRUCTURAL equation modeling , *MAGNETIC resonance imaging , *UNHEALTHY lifestyles , *ALZHEIMER'S disease - Abstract
Background: This work aimed to investigate the potential pathways involved in the association between social and lifestyle factors, biomarkers of Alzheimer's disease and related dementia (ADRD), and cognition. Methods: The authors studied 2323 participants from the Memento study, a French nationwide clinical cohort. Social and lifestyle factors were education level, current household incomes, physical activity, leisure activities, and social network from which two continuous latent variables were computed: an early to midlife (EML) and a latelife (LL) indicator. Brain magnetic resonance imaging (MRI), lumbar puncture, and amyloid-positron emission tomography (PET) were used to define three latent variables: neurodegeneration, small vessel disease (SVD), and AD pathology. Cognitive function was defined as the underlying factor of a latent variable with four cognitive tests. Structural equation models were used to evaluate cross-sectional pathways between social and lifestyle factors and cognition. Results: Participants' mean age was 70.9 years old, 62% were women, 28% were apolipoprotein-ε4 carriers, and 59% had a Clinical Dementia Rating (CDR) score of 0.5. Higher early to midlife social indicator was only directly associated with better cognitive function (direct β = 0.364 (0.322; 0.405), with no indirect pathway through ADRD biomarkers (total β = 0.392 (0.351; 0.429)). In addition to a direct effect on cognition (direct β = 0.076 (0.033; 0.118)), the association between latelife lifestyle indicator and cognition was also mostly mediated by an indirect effect through lower neurodegeneration (indirect β = 0.066 (0.042; 0.090) and direct β = − 0.116 (− 0.153; − 0.079)), but not through AD pathology nor SVD. Conclusions: Early to midlife social factors are directly associated with higher cognitive functions. Latelife lifestyle factors may help preserve cognitive functions through lower neurodegeneration. [ABSTRACT FROM AUTHOR]
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- 2022
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211. Neuroinflammation PET imaging of the translocator protein (TSPO) in Alzheimer's disease: An update.
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Gouilly, Dominique, Saint‐Aubert, Laure, Ribeiro, Maria‐Joao, Salabert, Anne‐Sophie, Tauber, Clovis, Péran, Patrice, Arlicot, Nicolas, Pariente, Jérémie, and Payoux, Pierre
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TRANSLOCATOR proteins , *POSITRON emission tomography , *ALZHEIMER'S disease , *NEUROINFLAMMATION - Abstract
Neuroinflammation is a significant contributor to Alzheimer's disease (AD). Until now, PET imaging of the translocator protein (TSPO) has been widely used to depict the neuroimmune endophenotype of AD. The aim of this review was to provide an update to the results from 2018 and to advance the characterization of the biological basis of TSPO imaging in AD by re‐examining TSPO function and expression and the methodological aspects of interest. Although the biological basis of the TSPO PET signal is obviously related to microglia and astrocytes in AD, the observed process remains uncertain and might not be directly related to neuroinflammation. Further studies are required to re‐examine the cellular significance underlying a variation in the PET signal in AD. [ABSTRACT FROM AUTHOR]
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- 2022
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212. Taking the A Train? Limited Consistency of Aβ42 and the Aβ42/40 Ratio in the AT(N) Classification.
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Gouilly, Dominique, Tisserand, Camille, Nogueira, Leonor, Saint-Lary, Laura, Rousseau, Vanessa, Benaiteau, Marie, Rafiq, Marie, Carlier, Jasmine, Milongo-Rigal, Emilie, Pagès, Jean-Christophe, and Pariente, Jérémie
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ALZHEIMER'S patients , *ALZHEIMER'S disease , *CEREBROSPINAL fluid , *CLASSIFICATION - Abstract
The consistency of cerebrospinal fluid amyloid-β (Aβ)42/40 ratio and Aβ42 has not been assessed in the AT(N) classification system. We analyzed the classification changes of the dichotomized amyloid status (A+/A-) in 363 patients tested for Alzheimer's disease biomarkers after Aβ42 was superseded by the Aβ42/40 ratio. The consistency of Aβ42 and the Aβ42/40 ratio was very low. Notably, the proportions of "false" A+T-patients were considerable (74-91%) and corresponded mostly to patients not clinically diagnosed with Alzheimer's disease. Our results suggest that the interchangeability of Aβ42/40 ratio and Aβ42 is limited for classifying patients in clinical setting using the AT(N) scheme. [ABSTRACT FROM AUTHOR]
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- 2021
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213. Language Network Connectivity Increases in Early Alzheimer's Disease.
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Pistono, Aurélie, Senoussi, Mehdi, Guerrier, Laura, Rafiq, Marie, Giméno, Mélanie, Péran, Patrice, Jucla, Mélanie, Pariente, Jérémie, and Gimeno, Mélanie
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ALZHEIMER'S disease , *TEMPORAL lobe , *MILD cognitive impairment , *BILINGUALISM , *FUNCTIONAL connectivity , *UNIVARIATE analysis , *BRAIN , *EXECUTIVE function , *RESEARCH , *NEURAL pathways , *RESEARCH methodology , *LANGUAGE & languages , *MAGNETIC resonance imaging , *MEDICAL cooperation , *EVALUATION research , *NEUROPSYCHOLOGICAL tests , *COMPARATIVE studies , *SPEECH , *NEUROLOGIC examination - Abstract
Background: Language production deficits occur early in the course of Alzheimer's disease (AD); however, only a few studies have focused on language network's functional connectivity in mild cognitive impairment (MCI) due to AD.Objective: The current study aims to uncover the extent of language alteration at the MCI stage, at a behavioral and neural level, using univariate and multivariate analyses of structural MRI and resting-state fMRI.Methods: Twenty-four MCI due to AD participants and 24 matched healthy controls underwent a comprehensive language evaluation, a structural T1-3D MRI, and resting-state fMRI. We performed seed-based analyses, using the left inferior frontal gyrus and left posterior temporal gyrus as seeds. Then, we analyzed connectivity between executive control networks and language network in each group. Finally, we used multivariate pattern analyses to test whether the two groups could be distinguished based on the pattern of atrophy within the language network; within the executive control networks, as well as the pattern of functional connectivity within the language network and within the executive control networks.Results: MCI due to AD participants had language impairment during standardized language tasks and connected-speech production. Regarding functional connectivity, univariate analyses were not able to discriminate participants, while multivariate pattern analyses could significantly predict participants' group. Language network's functional connectivity could discriminate MCI due to AD participants better than executive control networks. Most notably, they revealed an increased connectivity at the MCI stage, positively correlated with language performance.Conclusion: Multivariate analyses represent a useful tool for investigating the functional and structural (re-)organization of the neural bases of language. [ABSTRACT FROM AUTHOR]- Published
- 2021
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214. The long-term impact of irradiation on functional connectivity in brain circuits involved in memory processes after pediatric posterior fossa tumor.
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BAUDOU, Eloïse, PERAN, Patrice, TENSAOUTI, Fatima, ARRIBARAT, Germain, PARIENTE, Jérémie, COURBIERES, Nicolas, POLLIDORO, Lisa, BERTOZZI, Anne-Isabelle, GAMBART, Marion, SEVELY, Annick, ROQUES, Margaux, DUCASSOU, Anne, DANNA, Jérémy, TALLET, Jessica, DUFOUR, Christelle, CHAIX, Yves, and LAPRIE, Anne
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INFRATENTORIAL brain tumors , *COGNITIVE processing speed , *LONG-term memory , *EPISODIC memory , *FUNCTIONAL magnetic resonance imaging , *FUNCTIONAL connectivity - Abstract
[Display omitted] • Posterior fossa tumors and surgery have an impact on cortico-cerebellar connectivity. • Irradiation has an adding impact on cortico-hippocampal and -striatal connectivity. • Atypical connectivities are linked with memory outcomes in irradiated patients. • Hippocampus, striatum and cerebellum can be considered as organ at risk for memory. Memory is one of the main specific cognitive domains impaired with attention and processing speed after a pediatric brain tumor. This work explored the long-term impact of radiotherapy in children with posterior fossa tumor (PFT) on brain connectivity in neural circuits involved in memory using resting-state functional magnetic resonance imaging (rs-fMRI). A total of 20 irradiated and 15 non-irradiated PFT survivors, and 21 healthy controls, prospectively included in the IMPALA study (NCT04324450), performed memory tests assessing episodic, procedural, and working memories and were subjected to an rs-fMRI. We manually contoured main structures involved in memory to explore connectivity at rest in a seed-to-voxel analysis. The groups were compared and differences in connectivity were correlated with behavioral scores and irradiation doses. The performance of all mnesic tasks was lower in PFT survivors with a greater alteration in working and episodic memory in irradiated patients. Irradiated survivors had atypical connectivities in all memory circuits compared to controls and in cortico-caudate and cortico-cerebellar circuits compared to non-irradiated survivors. Non-irradiated survivors had only atypical connectivities in the cortico-cerebellar circuits compared to controls. In irradiated survivors, atypical connectivities in cortico-hippocampal circuits were linked with episodic memory scores and dose of irradiation to the left hippocampus and in cortico-striatal circuits with procedural memory scores and dose of irradiation to the striatum. The results of this study highlight that irradiation has a long-term impact on brain connectivity in brain circuits involved in memory after pediatric PFT with a specific radiation-dose effect in supratentorial structures. [ABSTRACT FROM AUTHOR]
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- 2024
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215. Increased functional connectivity supports language performance in healthy aging despite gray matter loss.
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Pistono, Aurélie, Guerrier, Laura, Péran, Patrice, Rafiq, Marie, Giméno, Mélanie, Bézy, Catherine, Pariente, Jérémie, and Jucla, Mélanie
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AGING , *GRAY matter (Nerve tissue) , *FUNCTIONAL connectivity , *FUNCTIONAL magnetic resonance imaging , *OLDER people , *NEUROLINGUISTICS - Abstract
Although language is quite preserved from aging, it remains unclear whether age-related differences lead to a deterioration or reorganization in language functional networks, or to different dynamics with other domains (e.g., the multiple-demand system). The present study is aimed at examining language networks, using resting-state functional magnetic resonance imaging in typical aging in relation to language performance. Twenty-three (23) younger adults and 24 healthy older adults were recruited. Volumetric gray matter differences between the 2 groups were assessed using voxel-based morphometry. Then, seed-based analyses, integrated local correlations in core regions of the language network, and within- and between-network connectivity were performed. We expected less extended connectivity maps, local coherence diminution, and higher connectivity with the multiple-demand system in older adults. On the contrary, analyses showed language network differences in healthy aging (i.e., increased connectivity with areas inside and outside language network), but no deterioration, despite widespread atrophy in older adults. Integrated local correlation revealed alterations that were unnoticeable with other analyses. Although gray matter loss was not correlated with language performance, connectivity differences were positively correlated with fluency performance in the older group. These results differ from the literature concerning other cognitive networks in aging in that they show extra internetwork connections without a decrease in intranetwork language connections. This reorganization could explain older adults' good language performance and could be interpreted in accordance with the scaffolding theory of aging and cognition. • Despite widespread atrophy older adults have minimal language functional network changes. • Local connectivity is reduced in language network during typical aging. • Age-related differences in language network are correlated with fluency performance. [ABSTRACT FROM AUTHOR]
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- 2021
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216. Post-stroke remodeling processes in animal models and humans.
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Cirillo, Carla, Brihmat, Nabila, Castel-Lacanal, Evelyne, Le Friec, Alice, Barbieux-Guillot, Marianne, Raposo, Nicolas, Pariente, Jérémie, Viguier, Alain, Simonetta-Moreau, Marion, Albucher, Jean-François, Olivot, Jean-Marc, Desmoulin, Franck, Marque, Philippe, Chollet, François, and Loubinoux, Isabelle
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After cerebral ischemia, events like neural plasticity and tissue reorganization intervene in lesioned and non-lesioned areas of the brain. These processes are tightly related to functional improvement and successful rehabilitation in patients. Plastic remodeling in the brain is associated with limited spontaneous functional recovery in patients. Improvement depends on the initial deficit, size, nature and localization of the infarction, together with the sex and age of the patient, all of them affecting the favorable outcome of reorganization and repair of damaged areas. A better understanding of cerebral plasticity is pivotal to design effective therapeutic strategies. Experimental models and clinical studies have fueled the current understanding of the cellular and molecular processes responsible for plastic remodeling. In this review, we describe the known mechanisms, in patients and animal models, underlying cerebral reorganization and contributing to functional recovery after ischemic stroke. We also discuss the manipulations and therapies that can stimulate neural plasticity. We finally explore a new topic in the field of ischemic stroke pathophysiology, namely the brain-gut axis. [ABSTRACT FROM AUTHOR]
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- 2020
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217. Grey Matter changes in treatment-resistant depression during electroconvulsive therapy.
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Yrondi, Antoine, Nemmi, Federico, Billoux, Sophie, Giron, Aurélie, Sporer, Marie, Taib, Simon, Salles, Juliette, Pierre, Damien, Thalamas, Claire, Rigal, Emilie, Danet, Lola, Pariente, Jérémie, Schmitt, Laurent, Arbus, Christophe, and Péran, Patrice
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ELECTROCONVULSIVE therapy , *HAMILTON Depression Inventory , *VISUAL fields , *FUSIFORM gyrus , *TEMPORAL lobe - Abstract
Introduction: 20-30% of depressed patients experience Treatment Resistant Depression (TRD). Electroconvulsive Therapy (ECT) remains the treatment of choice for TRD. However, the exact mechanism of ECT remains unclear. We aim to assess grey matter changes in patients with TRD undergoing bilateral ECT treatment at different points during and after treatment.Methods: Patients are recruited at the University Hospital of Toulouse. Eligibility criteria include a diagnosis of TRD and an age between 50 and 70 years old. Patients received clinical assessments (Hamilton Depression Rating Scale) and structural scans (MRI) at three points: baseline (within 48 h before the first ECT); V2 (after the first ECT considered effective); and V3 (within 1 week of completing ECT).Results: At baseline, controls had significantly higher cortical thickness than patients in the fusiform gyrus, the inferior, middle and superior temporal gyrus, the parahippocampal gyrus and the transverse temporal gyrus (respectively: t(35)=2.7, p = 0.02; t(35)=2.89, p = 0.017; t(35)=3.1, p = 0.015; t(35)=3.6, p = 0.009; t(35)=2.37, p = 0.031; t(35)=2.46, p = 0.03). This difference was no longer significant after ECT. We showed an increase in cortical thickness in superior temporal gyrus between (i) baseline and V3 (t(62)=-3.43 p = 0.009) and (ii) V2 and V3 (t(62)=-3.42 p = 0.009). We showed an increase in hippocampal volume between (i) baseline and V3 (t(62)=-5.23 p < 0.001) and (ii) V2 and V3 (t(62)=-5.3 p < 0.001).Conclusion: We highlight that there are grey matter changes during ECT treatment in a population with TRD compared to a healthy control population. These changes seem to occur after several rounds of ECT. [ABSTRACT FROM AUTHOR]- Published
- 2019
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218. Enlarged perivascular spaces and florbetapir uptake in patients with intracerebral hemorrhage.
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Raposo, Nicolas, Planton, Mélanie, Payoux, Pierre, Péran, Patrice, Albucher, Jean François, Calviere, Lionel, Viguier, Alain, Rousseau, Vanessa, Hitzel, Anne, Chollet, François, Olivot, Jean Marc, Bonneville, Fabrice, and Pariente, Jérémie
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POSITRON emission tomography , *CEREBRAL amyloid angiopathy , *BASAL ganglia , *HEMORRHAGE - Abstract
Purpose: Enlarged perivascular spaces in the centrum semiovale (CSO-EPVS) have been linked to cerebral amyloid angiopathy (CAA). To get insight into the underlying mechanisms of this association, we investigated the relationship between amyloid-β deposition assessed by 18F-florbetapir PET and CSO-EPVS in patients with acute intracerebral hemorrhage (ICH). Methods: We prospectively enrolled 18 patients with lobar ICH (suggesting CAA) and 20 with deep ICH (suggesting hypertensive angiopathy), who underwent brain MRI and 18F-florbetapir PET. EPVS were assessed on MRI using a validated 4-point visual rating scale in the centrum semiovale and the basal ganglia (BG-EPVS). PET images were visually assessed, blind to clinical and MRI data. We evaluated the association between florbetapir PET positivity and high degree (score> 2) of CSO-EPVS and BG-EPVS. Results: High CSO-EPVS degree was more common in patients with lobar ICH than deep ICH (55.6% vs. 20.0%; p = 0.02). Eight (57.1%) patients with high CSO-EPVS degree had a positive florbetapir PET compared with 4 (16.7%) with low CSO-EPVS degree (p = 0.01). In contrast, prevalence of florbetapir PET positivity was similar between patients with high vs. low BG-EPVS. In multivariable analysis adjusted for age, hypertension, and MRI markers of CAA, florbetapir PET positivity (odds ratio (OR) 6.44, 95% confidence interval (CI) 1.32–38.93; p = 0.03) was independently associated with high CSO-EPVS degree. Conclusions: Among patients with spontaneous ICH, high degree of CSO-EPVS but not BG-EPVS is associated with amyloid PET positivity. The findings provide further evidence that CSO-EPVS are markers of vascular amyloid burden that may be useful in diagnosing CAA. [ABSTRACT FROM AUTHOR]
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- 2019
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219. Clinical Effect of Early vs Late Amyloid Positron Emission Tomography in Memory Clinic Patients: The AMYPAD-DPMS Randomized Clinical Trial
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Altomare, Daniele, Barkhof, Frederik, Moro, Christian, Delrieu, Julien, Payoux, Pierre, Saint-Aubert, Laure, Hitzel, Anne, Molinuevo, José Luis, Grau-Rivera, Oriol, Gispert, Juan Domingo, Drzezga, Alexander, Jessen, Frank, Caprioglio, Camilla, Zeyen, Philip, Nordberg, Agneta, Savitcheva, Irina, Jelic, Vesna, Walker, Zuzana, Edison, Paul, Demonet, Jean-François, Gismondi, Rossella, Farrar, Gill, Stephens, Andrew W, Collij, Lyduine E, Frisoni, Giovanni B, Disease, Amyloid Imaging to Prevent Alzheimer’s, Scheltens, Philip, Lopes Alves, Isadora, Bouwman, Femke, Berkhof, Johannes, van Maurik, Ingrid S, Garibotto, Valentina, Cuevas, Rosario, Cufi, Marie-Noëlle, Dardenne, Sophie, de Arriba, Maria, de Costa Luis, Casper, de Gier, Yvonne, de Verbizier Lonjon, Delphine, Dekker, Veronique, Dekyndt, Bérengère, Delbeuck, Xavier, Delrieu, Julien, Demonet, Jean-François, Deramecourt, Vincent, Desclaux, Françoise, Diaz, Carlos, Diego, Susana, Djafar, Mehdi, Dölle, Britta, Doull, Laura, Dricot, Laurence, Drzezga, Alexander, Dubois, Bruno, Dumont, Julien, Dumur, Jean, Dumurgier, Julien, Dvorak, Martin, Ecay, Mirian, Edison, Paul, Escher, Claus, Estanga, Ainara, Esteban, Ester, Fanjaud, Guy, Farrar, Gill, Fauria, Karine, Felez Sanchez, Marta, Feukam Talla, Patrick, Ford, Lisa, Frisoni, Giovanni B, Fuster, David, Gabelle, Audrey, Garibotto, Valentina, Gaubert, Sinead, Gauci, Cédric, Geldhof, Christine, Georges, Jean, Ghika, Joseph, Gismondi, Rossella, Gispert, Juan Domingo, González, Elena, Goovaerts, Valerie, Goulart, Denis Mariano, Grasselli, Caroline, Grau-Rivera, Oriol, Gray, Katherine, Greensmith, Martin, Grozn, Laure, Guillemaud, Céline, Gunn, Fiona, Guntur Ramkumar, Prasad, Hagman, Göran, Hansseuw, Bernard, Heeman, Fiona, Hendriks, Janine, Himmelmann, Jakob, Hitzel, Anne, Hives, Florent, Hoenig, Merle, Hourrègue, Claire, Hudson, Justine, Huguet, Jordi, Ibarria, Marta, Iidow, Ifrah, Indart, Sandrine, Ingala, Silvia, Ivanoiu, Adrian, Jacquemont, Charlotte, Jelic, Vesna, Jessen, Frank, Jiao, Jieqing, Jofresa, Sara, Jonsson, Cathrine, Kaliukhovich, Dzmitry, Kern, Silke, Kivipelto, Miia, Knezevic, Iva, Kuchcinski, Grégory, Laforce, Manon, Lafuente, Asunción, Lala, Françoise, Lammertsma, Adriaan, Lax, Michelle, Lebouvier, Thibaud, Lee, Ho-Yun, Lee, Lean, Leeuwis, Annebet, Lefort, Amandine, Legrand, Jean-François, Leroy, Mélanie, Lesoil Markowski, Constance, Levy, Marcel, Lhommel, Renaud, Lopes, Renaud, Lopes Alves, Isadora, Lorenzini, Luigi, Lorette, Adrien, Luckett, Emma, Lundin, Marie, Mackowiak, Marie-Anne, Malotaux, Vincent, Manber, Richard, Manyakov, Nikolay, Markiewicz, Pawel, Marne, Paula, Marquié, Marta, Martín, Elvira, Martínez, Joan, Martinez Lage, Pablo, Mastenbroek, Sophie E, Maureille, Aurélien, Meersmans, Karen, Mett, Anja, Milne, Joseph, Minguillón, Carolina, Modat, Marc, Molinuevo, José Luis, Montrreal, Laura, Moro, Christian, Müller, Theresa, Muniz, Graciela, Mutsarts, Henk Jan, Nilsson, Ted, Ninerola, Aida, Nordberg, Agneta, Novaes, Wilse, Nuno Carmelo Pires Silva, Joao, Operto, Greg, Orellana, Adela, Ousset, Pierre-Jean, Outteryck, Olivier, Pallardy, Amandine, Palombit, Alessandro, Pancho, Ana, Pappon, Martin, Paquet, Claire, Pariente, Jérémie, Pasquier, Florence, Payoux, Pierre, Peaker, Harry, Pelejà, Esther, Pennetier, Delphine, Pérez-Cordón, Alba, Perissinotti, Andrés, Perrenoud, Matthieu Paul, Petit, Sandrine, Petyt, Grégory, Pfeil, Julia, Pirotte, Blanche, Pla, Sandra, Plaza Wuthrich, Sonia, Poitrine, Lea, Pollet, Marianne, Poncelet, Jean-Benoit, Prior, John, Pruvo, Jean-Pierre, Putallaz, Pauline, Queneau, Mathieu, Quenon, Lisa, Rădoi, Andreea, Rafiq, Marie, Ramage, Fiona, Ramis, Maribel, Reinwald, Michael, Rios, Gonzalo, Ritchie, Craig, Rodriguez, Elena, Rollin, Adeline, Rouaud, Olivier, Sacuiu, Simona, Saint-Aubert, Laure, Sala, Arianna, Salabert, Anne-Sophie, Saldias, Jon, Salvadó, Gemma, Sanabria, Angela, Sannemann, Lena, Sastre, Nathalie, Savina, Daniela, Savitcheva, Irina, Schaeverbeke, Jolien, Scheltens, Philip, Schildermans, Carine, Schmidt, Mark, Schöll, Michael, Schuermans, Jeroen, Semah, Franck, Shekari, Mahnaz, Skoog, Ingmar, Sotolongo-Grau, Oscar, Stephens, Andrew, Stewart, Tiffany, Stutzmann, Jennyfer, Tait, Murray, Tárraga, Lluis, Tartari, Juan Pablo, Tysen-Backstrom, Ann-Christine, Valero, Sergi, Vallez Garcia, David, van Berckel, Bart N M, van Essen, Martijn, Van Laere, Koen, van Leur, Jeroen, van Maurik, Ingrid S, Vandenberghe, Rik, Vellas, Bruno, Virolinen, Jukka, Visser, Pieter Jelle, Walker, Zuzana, Walles, Håkan, Wallin, Emilia, Whitelaw, Grant, Abdelnour, Carla, Wimberley, Catriona, Win, Zarni, Wink, Alle Meije, Wolz, Robin, Woodside, John, Yaqub, Maqsood, Zettergren, Anna, Zeyen, Philip, Aguilera, Nuria, Aksman, Leon, Alarcón-Martín, Emilio, Alegret, Montse, Alonso-Lana, Silvia, Altomare, Daniele, Andersen, Pia, Arab, Majd, Aspö, Malin, Bader, Ilona, Bader, Ilse, Banton, Nigel, Barkhof, Frederik, Barnes, Rodrigo, Barrie, Dawn, Battle, Mark, Belén Collado, Ana, Bellet, Julie, Berkhof, Johannes, Biger, Marine, Birck, Cindy, Bischof, Gerard, Boada, Mercè, Boellaard, Ronald, Bogdanovic, Nenad, Bollack, Ariane, Bombois, Stéphanie, Borg, Stefan, Borjesson-Hanson, Anne, Boskov, Vladimir, Boutantin, Justine, Boutoleau-Bretonniere, Claire, Bouwman, Femke, Breuilh, Laetitia, Bringman, Eva, Brunel, Baptiste, Bucci, Marco, Buckley, Chris, Buendía, Mar, Bullich, Santi, Calvet, Anna, Cañada, Laia, Cañada, Marta, Caprioglio, Camilla, Cardoso, Jorge, Carlier, Jasmine, Carre, Elise, Carrie, Isabelle, Cassagnaud, Pascaline, Cassol, Emmanuelle, Castilla-Martí, Miguel, Cazalon, Elodie, Chaarriau, Tiphaine, Chaigeau, Rachel, Chalmers, Taylor, Clerc, Marie-Thérèse, Clerigue, Montserrat, Cognat, Emmanuel, Coll, Nina, Collij, Lyduine E, Connely, Peter, Cordier, Elodie, Costes, Corine, Coulange, Camille, Courtemanche, Hélène, Creisson, Eric, and Crinquette, Charlotte
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Male ,Amyloid ,psychology [Alzheimer Disease] ,Amyloid beta-Peptides ,metabolism [Amyloid beta-Peptides] ,Amyloidogenic Proteins ,metabolism [Brain] ,Positron-Emission Tomography ,Humans ,Female ,Cognitive Dysfunction ,ddc:610 ,Prospective Studies ,3-(3,5-dichlorophenyl)-1-methyl-2,5-pyrrolidinedione ,Aged ,metabolism [Amyloid] - Abstract
Amyloid positron emission tomography (PET) allows the direct assessment of amyloid deposition, one of the main hallmarks of Alzheimer disease. However, this technique is currently not widely reimbursed because of the lack of appropriately designed studies demonstrating its clinical effect.To assess the clinical effect of amyloid PET in memory clinic patients.The AMYPAD-DPMS is a prospective randomized clinical trial in 8 European memory clinics. Participants were allocated (using a minimization method) to 3 study groups based on the performance of amyloid PET: arm 1, early in the diagnostic workup (within 1 month); arm 2, late in the diagnostic workup (after a mean [SD] 8 [2] months); or arm 3, if and when the managing physician chose. Participants were patients with subjective cognitive decline plus (SCD+; SCD plus clinical features increasing the likelihood of preclinical Alzheimer disease), mild cognitive impairment (MCI), or dementia; they were assessed at baseline and after 3 months. Recruitment took place between April 16, 2018, and October 30, 2020. Data analysis was performed from July 2022 to January 2023.Amyloid PET.The main outcome was the difference between arm 1 and arm 2 in the proportion of participants receiving an etiological diagnosis with a very high confidence (ie, ≥90% on a 50%-100% visual numeric scale) after 3 months.A total of 844 participants were screened, and 840 were enrolled (291 in arm 1, 271 in arm 2, 278 in arm 3). Baseline and 3-month visit data were available for 272 participants in arm 1 and 260 in arm 2 (median [IQR] age: 71 [65-77] and 71 [65-77] years; 150/272 male [55%] and 135/260 male [52%]; 122/272 female [45%] and 125/260 female [48%]; median [IQR] education: 12 [10-15] and 13 [10-16] years, respectively). After 3 months, 109 of 272 participants (40%) in arm 1 had a diagnosis with very high confidence vs 30 of 260 (11%) in arm 2 (P < .001). This was consistent across cognitive stages (SCD+: 25/84 [30%] vs 5/78 [6%]; P < .001; MCI: 45/108 [42%] vs 9/102 [9%]; P < .001; dementia: 39/80 [49%] vs 16/80 [20%]; P < .001).In this study, early amyloid PET allowed memory clinic patients to receive an etiological diagnosis with very high confidence after only 3 months compared with patients who had not undergone amyloid PET. These findings support the implementation of amyloid PET early in the diagnostic workup of memory clinic patients.EudraCT Number: 2017-002527-21.
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- 2023
220. Neuronal spiking activity highlights a gradient of epileptogenicity in human tuberous sclerosis lesions.
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Despouy, Elodie, Curot, Jonathan, Denuelle, Marie, Deudon, Martin, Sol, Jean-Christophe, Lotterie, Jean-Albert, Reddy, Leila, Nowak, Lionel G., Pariente, Jérémie, Thorpe, Simon J., Valton, Luc, and Barbeau, Emmanuel J.
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ACTION potentials , *TUBEROUS sclerosis - Abstract
Highlights • First recordings of spiking neuronal activity in the tuber and perituberal tissue using new hybrid electrodes equipped with tetrodes. • Gradient of epileptogenicity running from the tuber to perituberal tissue revealed by multi-scale analyses. • Observation of interactions both within and between the tuber and perituber. Abstract Objective The mechanisms underlying epileptogenicity in tuberous sclerosis complex (TSC) are poorly understood. Methods We analysed neuronal spiking activity (84 neurons), fast ripples (FRs), local field potentials and intracranial electroencephalogram during interictal epileptiform discharges (IEDs) in the tuber and perituber of a patient using novel hybrid electrodes equipped with tetrodes. Results IEDs were recorded in the tuber and perituber. FRs were recorded only in the tuber and only with the microelectrodes. A larger proportion of neurons in the tuber (57%) than in the perituber (17%) had firing-rates modulated around IEDs. Conclusions A multi-scale analysis of neuronal activity, FRs and IEDs indicates a gradient of epileptogenicity running from the tuber to the perituber. Significance We demonstrate, for the first time in vivo , a gradient of epileptogenicity from the tuber to the perituber, which paves the way for future models of epilepsy in TSC. Our results also question the extent of the neurosurgical resection, including or not the perituber, that needs to be made in these patients. [ABSTRACT FROM AUTHOR]
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- 2019
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221. The Regulatory Role of the Human Mediodorsal Thalamus.
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Pergola, Giulio, Danet, Lola, Pitel, Anne-Lise, Carlesimo, Giovanni A., Segobin, Shailendra, Pariente, Jérémie, Suchan, Boris, Mitchell, Anna S., and Barbeau, Emmanuel J.
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THALAMUS , *BRAIN imaging , *PREFRONTAL cortex , *NEUROPSYCHOLOGICAL tests , *COGNITION - Abstract
The function of the human mediodorsal thalamic nucleus (MD) has so far eluded a clear definition in terms of specific cognitive processes and tasks. Although it was at first proposed to play a role in long-term memory, a set of recent studies in animals and humans has revealed a more complex, and broader, role in several cognitive functions. The MD seems to play a multifaceted role in higher cognitive functions together with the prefrontal cortex and other cortical and subcortical brain areas. Specifically, we propose that the MD is involved in the regulation of cortical networks especially when the maintenance and temporal extension of persistent activity patterns in the frontal lobe areas are required. Highlights The mediodorsal thalamic nucleus is involved in the cognitive deficits observed in several neurological and psychiatric disorders. The long-standing belief in a role of the mediodorsal thalamic nucleus mainly in long-term memory is now being reconsidered. Recent studies emphasize its function in many cognitive tasks related to the prefrontal cortex. The mediodorsal thalamic nucleus is required for the rapid and accurate performance of cognitive tasks and temporally extends the efficiency of cortical networks involving the prefrontal cortex. We propose that the common ground of multiple lines of evidence from human studies points to a role of the mediodorsal thalamic nucleus in regulating prefrontal activity patterns. These hypotheses can be tested by developing specific neuropsychological tasks, parceling the thalamus with high-resolution MRI, and using intracranial recordings in humans. [ABSTRACT FROM AUTHOR]
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- 2018
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222. N°383 – Sleep-related epileptic activities in Alzheimer disease are sparse and do not have a major impact on cognition.
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Szabo, Anna B., Curot, Jonathan, Denuelle, Marie, Debs, Rachel, Barbeau, Emmanuel, Lemesle, Béatrice, Gerard, Fleur, Péran, Patrice, Pariente, Jérémie, Dahan, Lionel, and Valton, Luc
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ALZHEIMER'S disease , *PEOPLE with epilepsy , *COGNITION - Published
- 2023
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223. Plasma lysosphingolipids in GRN-related diseases: Monitoring lysosomal dysfunction to track disease progression.
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Khrouf, Walid, Saracino, Dario, Rucheton, Benoit, Houot, Marion, Clot, Fabienne, Rinaldi, Daisy, Vitor, Joana, Huynh, Marie, Heng, Evelyne, Schlemmer, Dimitri, Pasquier, Florence, Deramecourt, Vincent, Auriacombe, Sophie, Azuar, Carole, Levy, Richard, Bombois, Stéphanie, Boutoleau-Brétonnière, Claire, Pariente, Jérémie, Didic, Mira, and Wallon, David
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DISEASE progression , *FRONTOTEMPORAL dementia , *PLASMA displays , *GLYCOGEN storage disease type II , *MASS spectrometry , *LYSOSOMAL storage diseases - Abstract
GRN mutations are among the main genetic causes of frontotemporal dementia (FTD). Considering the progranulin involvement in lysosomal homeostasis, we aimed to evaluate if plasma lysosphingolipids (lysoSPL) are increased in GRN mutation carriers, and whether they might represent relevant fluid-based biomarkers in GRN -related diseases. We analyzed four lysoSPL levels in plasmas of 131 GRN carriers and 142 non-carriers, including healthy controls and patients with frontotemporal dementias (FTD) carrying a C9orf72 expansion or without any mutation. GRN carriers consisted of 102 heterozygous FTD patients (FTD- GRN), three homozygous patients with neuronal ceroid lipofuscinosis-11 (CLN-11) and 26 presymptomatic carriers (PS- GRN), the latter with longitudinal assessments. Glucosylsphingosin d18:1 (LGL1), lysosphingomyelins d18:1 and isoform 509 (LSM18:1, LSM509) and lysoglobotriaosylceramide (LGB3) were measured by electrospray ionization-tandem mass spectrometry coupled to ultraperformance liquid chromatography. Levels of LGL1, LSM18:1 and LSM509 were increased in GRN carriers compared to non-carriers (p < 0.0001). No lysoSPL increases were detected in FTD patients without GRN mutations. LGL1 and LSM18:1 progressively increased with age at sampling, and LGL1 with disease duration, in FTD- GRN. Among PS- GRN carriers, LSM18:1 and LGL1 significantly increased over 3.4-year follow-up. LGL1 levels were associated with increasing neurofilaments in presymptomatic carriers. This study evidences an age-dependent increase of β-glucocerebrosidase and acid sphingomyelinase substrates in GRN patients, with progressive changes as early as the presymptomatic phase. Among FTD patients, plasma lysoSPL appear to be uniquely elevated in GRN carriers, and thus might serve as suitable non-invasive disease-tracking biomarkers of progression, specific to the pathophysiological process. Finally, this study might add lysoSPL to the portfolio of fluid-based biomarkers, and pave the way to disease-modifying approaches based on lysosomal function rescue in GRN diseases. • GRN mutation carriers display increased plasma levels of lysosphingolipids (lysoSPL). • Lysosphingomyelins are elevated in presymptomatic (PS) and symptomatic carriers. • Glucosylsphingosine displays an age-dependent increase in GRN -associated FTD patients. • In PS carriers, LSM18:1 and LGL1 increase over time, in association with NfL changes. • Lysosomal biomarker dosages contribute to monitor disease progression in GRN carriers. [ABSTRACT FROM AUTHOR]
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- 2023
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224. Alteration of rhythmic unimanual tapping and anti-phase bimanual coordination in Alzheimer's disease: A sign of inter-hemispheric disconnection?
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Martin, Elodie, Blais, Mélody, Albaret, Jean-Michel, Pariente, Jérémie, and Tallet, Jessica
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ALZHEIMER'S disease , *CORPUS callosum , *NEUROPSYCHOLOGY , *PSYCHOLOGY of movement , *SYNCHRONIZATION , *BRAIN diseases , *ATTENTION , *CEREBRAL dominance , *CYCLES , *TIME , *TRANSFER of training , *BODY movement - Abstract
Little attention is paid to motor control in Alzheimer's disease (AD) although it is a relevant sign of central nervous system integrity and functioning. In particular, unimanual and bimanual tapping is a relevant paradigm because it requires intra- and inter-hemispheric transfer (IHT). Previous results indicate that both unimanual and anti-phase tapping requires more IHT than in-phase tapping, especially produced without external stimulation. The aim of the present study was to test the production of unimanual, bimanual in-phase and anti-phase tapping with a synchronization-continuation paradigm with and without visual stimulation in AD patients (N=9) and control participants (N=12). In accordance with our hypothesis, these results suggest that unimanual and anti-phase tapping is more altered in AD than in control participants. Moreover, performance is globally more variable in the AD group. These alterations are discussed in terms of possible IHT modulation, in line with functional and structural findings in AD, revealing changes in the connectivity of brain regions across hemispheres and white matter damage. [ABSTRACT FROM AUTHOR]
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- 2017
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225. Familiarity and recollection vs representational models of medial temporal lobe structures: A single-case study.
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Lacot, Emilie, Vautier, Stéphane, Kőhler, Stefan, Pariente, Jérémie, Martin, Chris B., Puel, Michèle, Lotterie, Jean-Albert, and Barbeau, Emmanuel J.
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TEMPORAL lobe , *EXPLICIT memory , *NEURAL circuitry , *NEURAL transmission , *HIPPOCAMPUS (Brain) , *VISUAL perception - Abstract
Although it is known that medial temporal lobe (MTL) structures support declarative memory, the fact these structures have different architectonics and circuitry suggests they may also play different functional roles. Selective lesions of MTL structures offer an opportunity to understand these roles. We report, in this study, on JMG, a patient who presents highly unusual lesions that completely affected all MTL structures except for the right hippocampus and parts of neighbouring medial parahippocampal cortex. We first demonstrate that JMG shows preserved recall for visual material on 5 experimental tasks. This finding suggests that his right hippocampus is functional, even though it appears largely disconnected from most of its MTL afferents. In contrast, JMG performed very poorly, as compared to control subjects, on 7 tasks of visual recognition memory for single items. Although he sometimes performed above chance, neither familiarity nor recollection appeared fully preserved. These results indicate that extrahippocampal structures, damaged bilaterally in JMG, perform critical operations for item recognition; and that the hippocampus cannot take over that role, including recollection, when these structures are largely damaged. Finally, in a set of 3 recognition memory tasks with scenes as stimuli, JMG performed at the level of control participants and obtained normal indices of familiarity and recollection. Overall, our findings suggest that the right hippocampus and remnants of parahippocampal cortex can support recognition memory for scenes in the absence of preserved item-recognition memory. The patterns of dissociations, which we report in the present study, provide support for a representational account of the functional organization of MTL structures. [ABSTRACT FROM AUTHOR]
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- 2017
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226. Memory scrutinized through electrical brain stimulation: A review of 80 years of experiential phenomena.
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Curot, Jonathan, Busigny, Thomas, Valton, Luc, Denuelle, Marie, Vignal, Jean-Pierre, Maillard, Louis, Chauvel, Patrick, Pariente, Jérémie, Trebuchon, Agnès, Bartolomei, Fabrice, and Barbeau, Emmanuel J.
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BRAIN stimulation , *REMINISCENCE , *EPISODIC memory , *EXPLICIT memory , *PREDICTION models - Abstract
Electrical brain stimulations (EBS) sometimes induce reminiscences, but it is largely unknown what type of memories they can trigger. We reviewed 80 years of literature on reminiscences induced by EBS and added our own database. We classified them according to modern conceptions of memory. We observed a surprisingly large variety of reminiscences covering all aspects of declarative memory. However, most were poorly detailed and only a few were episodic. This result does not support theories of a highly stable and detailed memory, as initially postulated, and still widely believed as true by the general public. Moreover, memory networks could only be activated by some of their nodes: 94.1% of EBS were temporal, although the parietal and frontal lobes, also involved in memory networks, were stimulated. The qualitative nature of memories largely depended on the site of stimulation: EBS to rhinal cortex mostly induced personal semantic reminiscences, while only hippocampal EBS induced episodic memories. This result supports the view that EBS can activate memory in predictable ways in humans. [ABSTRACT FROM AUTHOR]
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- 2017
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227. Challenging diagnosis and treatment decision of a long-history autoantibody-negative autoimmune encephalitis.
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Calvat, Pauline, Leung, Clémence, Bost, Chloé, Fortenfant, Francoise, Simonetta-Moreau, Marion, Pariente, Jérémie, Rafiq, Marie, Brefel-Courbon, Christine, Rascol, Olivier, Fabbri, Margherita, and Ory-Magne, Fabienne
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ENCEPHALITIS , *DIAGNOSIS , *THERAPEUTICS , *ATAXIA , *DYSTONIA - Published
- 2023
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228. Primary Progressive Aphasia Associated With GRN Mutations: New Insights Into the Nonamyloid Logopenic Variant
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Bruno Dubois, Audrey Gabelle, François Sellal, Jérémie Pariente, Marie Sarazin, Agnès Camuzat, Raffaella Migliaccio, Frédérique Etcharry-Bouyx, Amandine Geraudie, Sophie Ferrieux, Simona Bottani, Carole Roué-Jagot, Mira Didic, Florence Pasquier, Leila Sellami, Alexis Brice, Olivier Colliot, Fabienne Clot, Marc Teichmann, Didier Hannequin, Christel Thauvin-Robinet, Claire Boutoleau-Bretonnière, Julien Lagarde, Cinzia Coppola, David Wallon, Richard Levy, Marie Noguès-Lassiaille, Dario Saracino, Aurélie Funkiewiez, Maria Luisa Gorno-Tempini, Olivier Martinaud, Isabelle Le Ber, Marion Houot, Stéphane Epelbaum, Sophie Auriacombe, Alexandre Morin, Vincent Deramecourt, Ftd-Als, Philippe Couratier, Daisy Rinaldi, Saracino, Dario, Ferrieux, Sophie, Noguès-Lassiaille, Marie, Houot, Marion, Funkiewiez, Aurélie, Sellami, Leila, Deramecourt, Vincent, Pasquier, Florence, Couratier, Philippe, Pariente, Jérémie, Géraudie, Amandine, Epelbaum, Stéphane, Wallon, David, Hannequin, Didier, Martinaud, Olivier, Clot, Fabienne, Camuzat, Agnè, Bottani, Simona, Rinaldi, Daisy, Auriacombe, Sophie, Sarazin, Marie, Didic, Mira, Boutoleau-Bretonnière, Claire, Thauvin-Robinet, Christel, Lagarde, Julien, Roué-Jagot, Carole, Sellal, Françoi, Gabelle, Audrey, Etcharry-Bouyx, Frédérique, Morin, Alexandre, Coppola, Cinzia, Levy, Richard, Dubois, Bruno, Brice, Alexi, Colliot, Olivier, Luisa Gorno-Tempini, Maria, Teichmann, Marc, Migliaccio, Raffaella, Le Ber, Isabelle, Institut du Cerveau = Paris Brain Institute (ICM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), CHU Lille, CHU Limoges, Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Algorithms, models and methods for images and signals of the human brain (ARAMIS), Sorbonne Université (SU)-Inria de Paris, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria)-Institut du Cerveau = Paris Brain Institute (ICM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Génomique et Médecine Personnalisée du Cancer et des Maladies Neuropsychiatriques (GPMCND), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Neuropsychologie et imagerie de la mémoire humaine (NIMH), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Charles Foix [AP-HP], Bordeaux population health (BPH), Université de Bordeaux (UB)-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Sainte Anne [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Hôpital de la Timone [CHU - APHM] (TIMONE), Institut de Neurosciences des Systèmes (INS), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre hospitalier universitaire de Nantes (CHU Nantes), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), GHU AP-HP Centre Université de Paris, Hôpitaux Civils de Colmar, Neuropsychiatrie : recherche épidémiologique et clinique (PSNREC), Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), University of the Study of Campania Luigi Vanvitelli, University of California [San Francisco] (UC San Francisco), University of California (UC), The research leading to these results received funding from the Investissements davenir ANR-11-INBS-0011. This work was funded by the Programme Hospitalier de Recherche Clinique (PHRC) FTLD-exome (to ILB, promotion by Assistance Publique Hôpitaux de Paris), PHRC Predict-PGRN (to ILB, promotion by Assistance Publique Hôpitaux de Paris)., ANR-11-INBS-0011,NeurATRIS,Infrastructure de Recherche Translationnelle pour les Biothérapies en Neurosciences(2011), ANR-19-P3IA-0001,PRAIRIE,PaRis Artificial Intelligence Research InstitutE(2019), Admin, Oskar, Infrastructures - Infrastructure de Recherche Translationnelle pour les Biothérapies en Neurosciences - - NeurATRIS2011 - ANR-11-INBS-0011 - INBS - VALID, PaRis Artificial Intelligence Research InstitutE - - PRAIRIE2019 - ANR-19-P3IA-0001 - P3IA - VALID, Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), CHU Toulouse [Toulouse], Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria)-Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL), Université Montpellier 1 (UM1)-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM), University of California [San Francisco] (UCSF), University of California, Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), and Normandie Université (NU)-Normandie Université (NU)-École Pratique des Hautes Études (EPHE)
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Oncology ,medicine.medical_specialty ,Apraxia ,050105 experimental psychology ,Primary progressive aphasia ,03 medical and health sciences ,Dementia aphasia ,0302 clinical medicine ,Atrophy ,Gyrus ,Aphasia ,Agrammatism ,Internal medicine ,medicine ,0501 psychology and cognitive sciences ,Prospective cohort study ,business.industry ,05 social sciences ,respiratory system ,medicine.disease ,medicine.anatomical_structure ,[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie ,[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie ,Neurology (clinical) ,medicine.symptom ,business ,030217 neurology & neurosurgery ,Frontotemporal dementia - Abstract
ObjectiveTo determine relative frequencies and linguistic profiles of primary progressive aphasia (PPA) variants associated with GRN (progranulin) mutations and to study their neuroanatomic correlates.MethodsPatients with PPA carrying GRN mutations (PPA-GRN) were selected among a national prospective research cohort of 1,696 patients with frontotemporal dementia, including 235 patients with PPA. All patients with amyloid-positive CSF biomarkers were excluded. In this cross-sectional study, speech/language and cognitive profiles were characterized with standardized evaluations, and gray matter (GM) atrophy patterns using voxel-based morphometry. Comparisons were performed with controls and patients with sporadic PPA.ResultsAmong the 235 patients with PPA, 45 (19%) carried GRN mutations, and we studied 32 of these. We showed that logopenic PPA (lvPPA) was the most frequent linguistic variant (n = 13, 41%), followed by nonfluent/agrammatic (nfvPPA; n = 9, 28%) and mixed forms (n = 8, 25%). Semantic variant was rather rare (n = 2, 6%). Patients with lvPPA, qualified as nonamyloid lvPPA, presented canonical logopenic deficit. Seven of 13 had a pure form; 6 showed subtle additional linguistic deficits not fitting criteria for mixed PPA and hence were labeled as logopenic-spectrum variant. GM atrophy involved primarily left posterior temporal gyrus, mirroring neuroanatomic changes of amyloid-positive-lvPPA. Patients with nfvPPA presented agrammatism (89%) rather than apraxia of speech (11%).ConclusionsThis study shows that the most frequent PPA variant associated with GRN mutations is nonamyloid lvPPA, preceding nfvPPA and mixed forms, and illustrates that the language network may be affected at different levels. GRN testing is indicated for patients with PPA, whether familial or sporadic. This finding is important for upcoming GRN gene–specific therapies.
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- 2021
229. The Rise of the GRN C157KfsX97 Mutation in Southern Italy: Going Back to the Fall of the Western Roman Empire
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Veronica Redaelli, Giorgio Giaccone, Isabelle Le Ber, Giacomina Rossi, Jérémie Pariente, Matteo Carrara, Luisa Benussi, Pietro Tiraboschi, Martina Ricci, Gianfranco Puoti, Simona Bonavita, Mariano Oliva, Giacomo Lus, Cinzia Coppola, Alessandro Tessitore, Dario Saracino, Paola Caroppo, Roberta Ghidoni, Coppola, Cinzia, Saracino, Dario, Oliva, Mariano, Puoti, Gianfranco, Lus, Giacomo, Le Ber, Isabelle, Pariente, Jérémie, Tessitore, Alessandro, Benussi, Luisa, Ghidoni, Roberta, Carrara, Matteo, Ricci, Martina, Redaelli, Veronica, Tiraboschi, Pietro, Caroppo, Paola, Giaccone, Giorgio, Bonavita, Simona, and Rossi, Giacomina
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Most recent common ancestor ,Male ,haplotype ,Common founder ,Genetic counseling ,Population ,Biology ,Roman World ,Cohort Studies ,Progranulins ,mental disorders ,mutation dating ,medicine ,Humans ,education ,Aged ,Genetics ,education.field_of_study ,Genetic heterogeneity ,General Neuroscience ,Haplotype ,General Medicine ,Frontotemporal lobar degeneration ,Middle Aged ,medicine.disease ,nervous system diseases ,Psychiatry and Mental health ,Clinical Psychology ,Haplotypes ,Italy ,Mutation (genetic algorithm) ,Mutation ,Intercellular Signaling Peptides and Proteins ,Female ,Geriatrics and Gerontology ,Frontotemporal Lobar Degeneration ,GRN ,Founder effect - Abstract
Background: Frontotemporal lobar degeneration (FTLD) designates a group of neurodegenerative diseases with remarkable clinical, pathological, and genetic heterogeneity. Mutations in progranulin gene (GRN) are among the most common causes of familial FTLD. The GRN C157KfsX97 mutation is the most frequent mutation occurring in Southern Italy and has been already described in a previous work. Objective: In this study, we reported on additional cases carrying the same mutation and performed a genetic study on the whole cohort, aiming at demonstrating the existence of a founder effect and estimating the age of this mutation. Methods/Results: Based on the haplotype sharing analysis, a founder effect was highly probable, while the age of the mutation, estimated by means of DMLE+ software, resulted in a range between 52 and 82 generations, with the highest frequency at about 62 generations, 1,550 years ago. Conclusion: This is the first study that reports the age estimation of the most recent common ancestor for the GRN C157KfsX97 mutation recurring in Southern Italy. Mutation dating in a geographically restricted population may be useful in order to plan genetic counseling and screening programs in the field of public health.
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- 2020
230. Insight on AV-45 binding in white and grey matter from histogram analysis: a study on early Alzheimer's disease patients and healthy subjects.
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Nemmi, Federico, Saint-Aubert, Laure, Adel, Djilali, Salabert, Anne-Sophie, Pariente, Jérémie, Barbeau, Emmanuel, Payoux, Pierre, and Péran, Patrice
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ALZHEIMER'S patients , *HISTOGRAMS , *AMYLOID , *TOMOGRAPHY , *MAGNETIC resonance imaging - Abstract
Purpose: AV-45 amyloid biomarker is known to show uptake in white matter in patients with Alzheimer's disease (AD), but also in the healthy population. This binding, thought to be of a non-specific lipophilic nature, has not yet been investigated. The aim of this study was to determine the differential pattern of AV-45 binding in white matter in healthy and pathological populations. Methods: We recruited 24 patients presenting with AD at an early stage and 17 matched, healthy subjects. We used an optimized positron emission tomography-magnetic resonance imaging (PET-MRI) registration method and an approach based on an intensity histogram using several indices. We compared the results of the intensity histogram analyses with a more canonical approach based on target-to-cerebellum Standard Uptake Value (SUVr) in white and grey matter using MANOVA and discriminant analyses. A cluster analysis on white and grey matter histograms was also performed. Results: White matter histogram analysis revealed significant differences between AD and healthy subjects, which were not revealed by SUVr analysis. However, white matter histograms were not decisive to discriminate groups, and indices based on grey matter only showed better discriminative power than SUVr. The cluster analysis divided our sample into two clusters, showing different uptakes in grey, but also in white matter. Conclusion: These results demonstrate that AV-45 binding in white matter conveys subtle information not detectable using the SUVr approach. Although it is not more efficient than standard SUVr in discriminating AD patients from healthy subjects, this information could reveal white matter modifications. [ABSTRACT FROM AUTHOR]
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- 2014
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231. Phenotypic spectrum of probable and genetically-confirmed idiopathic basal ganglia calcification.
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Nicolas, Gaël, Pottier, Cyril, Charbonnier, Camille, Guyant-Maréchal, Lucie, Le Ber, Isabelle, Pariente, Jérémie, Labauge, Pierre, Ayrignac, Xavier, Defebvre, Luc, Maltête, David, Martinaud, Olivier, Lefaucheur, Romain, Guillin, Olivier, Wallon, David, Chaumette, Boris, Rondepierre, Philippe, Derache, Nathalie, Fromager, Guillaume, Schaeffer, Stéphane, and Krystkowiak, Pierre
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PHENOTYPES , *BASAL ganglia , *CALCIFICATION , *TOMOGRAPHY , *CALCIUM in the body , *BIOMINERALIZATION , *TEACHING hospitals - Abstract
Idiopathic basal ganglia calcification is characterized by mineral deposits in the brain, an autosomal dominant pattern of inheritance in most cases and genetic heterogeneity. The first causal genes, SLC20A2 and PDGFRB, have recently been reported. Diagnosing idiopathic basal ganglia calcification necessitates the exclusion of other causes, including calcification related to normal ageing, for which no normative data exist. Our objectives were to diagnose accurately and then describe the clinical and radiological characteristics of idiopathic basal ganglia calcification. First, calcifications were evaluated using a visual rating scale on the computerized tomography scans of 600 consecutively hospitalized unselected controls. We determined an age-specific threshold in these control computerized tomography scans as the value of the 99th percentile of the total calcification score within three age categories: <40, 40–60, and >60 years. To study the phenotype of the disease, patients with basal ganglia calcification were recruited from several medical centres. Calcifications that rated below the age-specific threshold using the same scale were excluded, as were patients with differential diagnoses of idiopathic basal ganglia calcification, after an extensive aetiological assessment. Sanger sequencing of SLC20A2 and PDGFRB was performed. In total, 72 patients were diagnosed with idiopathic basal ganglia calcification, 25 of whom bore a mutation in either SLC20A2 (two families, four sporadic cases) or PDGFRB (one family, two sporadic cases). Five mutations were novel. Seventy-one per cent of the patients with idiopathic basal ganglia calcification were symptomatic (mean age of clinical onset: 39 ± 20 years; mean age at last evaluation: 55 ± 19 years). Among them, the most frequent signs were: cognitive impairment (58.8%), psychiatric symptoms (56.9%) and movement disorders (54.9%). Few clinical differences appeared between SLC20A2 and PDGFRB mutation carriers. Radiological analysis revealed that the total calcification scores correlated positively with age in controls and patients, but increased more rapidly with age in patients. The expected total calcification score was greater in SLC20A2 than PDGFRB mutation carriers, beyond the effect of the age alone. No patient with a PDGFRB mutation exhibited a cortical or a vermis calcification. The total calcification score was more severe in symptomatic versus asymptomatic individuals. We provide the first phenotypical description of a case series of patients with idiopathic basal ganglia calcification since the identification of the first causative genes. Clinical and radiological diversity is confirmed, whatever the genetic status. Quantification of calcification is correlated with the symptomatic status, but the location and the severity of the calcifications don’t reflect the whole clinical diversity. Other biomarkers may be helpful in better predicting clinical expression. [ABSTRACT FROM PUBLISHER]
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- 2013
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232. Fluoxetine for motor recovery after acute ischaemic stroke (FLAME): a randomised placebo-controlled trial
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Chollet, François, Tardy, Jean, Albucher, Jean-François, Thalamas, Claire, Berard, Emilie, Lamy, Catherine, Bejot, Yannick, Deltour, Sandrine, Jaillard, Assia, Niclot, Philippe, Guillon, Benoit, Moulin, Thierry, Marque, Philippe, Pariente, Jérémie, Arnaud, Catherine, and Loubinoux, Isabelle
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FLUOXETINE , *PHYSIOLOGICAL therapeutics , *HEMIPLEGICS , *PARALYSIS , *PLACEBOS , *HEPATOTOXICOLOGY , *HEART diseases , *RANDOMIZED controlled trials , *CEREBROVASCULAR disease , *DRUG efficacy - Abstract
Summary: Background: Hemiplegia and hemiparesis are the most common deficits caused by stroke. A few small clinical trials suggest that fluoxetine enhances motor recovery but its clinical efficacy is unknown. We therefore aimed to investigate whether fluoxetine would enhance motor recovery if given soon after an ischaemic stroke to patients who have motor deficits. Methods: In this double-blind, placebo-controlled trial, patients from nine stroke centres in France who had ischaemic stroke and hemiplegia or hemiparesis, had Fugl-Meyer motor scale (FMMS) scores of 55 or less, and were aged between 18 years and 85 years were eligible for inclusion. Patients were randomly assigned, using a computer random-number generator, in a 1:1 ratio to fluoxetine (20 mg once per day, orally) or placebo for 3 months starting 5–10 days after the onset of stroke. All patients had physiotherapy. The primary outcome measure was the change on the FMMS between day 0 and day 90 after the start of the study drug. Participants, carers, and physicians assessing the outcome were masked to group assignment. Analysis was of all patients for whom data were available (full analysis set). This trial is registered with ClinicalTrials.gov, number NCT00657163. Findings: 118 patients were randomly assigned to fluoxetine (n=59) or placebo (n=59), and 113 were included in the analysis (57 in the fluoxetine group and 56 in the placebo group). Two patients died before day 90 and three withdrew from the study. FMMS improvement at day 90 was significantly greater in the fluoxetine group (adjusted mean 34·0 points [95% CI 29·7–38·4]) than in the placebo group (24·3 points [19·9–28·7]; p=0·003). The main adverse events in the fluoxetine and placebo groups were hyponatraemia (two [4%] vs two [4%]), transient digestive disorders including nausea, diarrhoea, and abdominal pain (14 [25%] vs six [11%]), hepatic enzyme disorders (five [9%] vs ten [18%]), psychiatric disorders (three [5%] vs four [7%]), insomnia (19 [33%] vs 20 [36%]), and partial seizure (one [<1%] vs 0). Interpretation: In patients with ischaemic stroke and moderate to severe motor deficit, the early prescription of fluoxetine with physiotherapy enhanced motor recovery after 3 months. Modulation of spontaneous brain plasticity by drugs is a promising pathway for treatment of patients with ischaemic stroke and moderate to severe motor deficit. Funding: Public French National Programme for Clinical Research. [Copyright &y& Elsevier]
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- 2011
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233. Plasma progranulin levels for frontotemporal dementia in clinical practice: a 10-year French experience.
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Sellami, Leila, Rucheton, Benoît, Ben Younes, Imen, Camuzat, Agnès, Saracino, Dario, Rinaldi, Daisy, Epelbaum, Stephane, Azuar, Carole, Levy, Richard, Auriacombe, Sophie, Hannequin, Didier, Pariente, Jérémie, Barbier, Mathieu, Boutoleau-Bretonnière, Claire, Couratier, Philippe, Pasquier, Florence, Deramecourt, Vincent, Sauvée, Mathilde, Sarazin, Marie, and Lagarde, Julien
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FRONTOTEMPORAL dementia , *FRONTOTEMPORAL lobar degeneration , *PROGRANULIN , *AGE of onset , *PATIENT-family relations - Abstract
GRN mutations are frequent causes of familial frontotemporal degeneration. Although there is no clear consensual threshold, plasma progranulin levels represent an efficient biomarker for predicting GRN mutations when decreased. We evaluated plasma levels to determine whether it could also predict age at onset, clinical phenotype, or disease progression in 160 GRN carriers. Importantly, progranulin levels were influenced by gender, with lower levels in male than in female patients in our study. Although we found no correlation with age at onset or with clinical phenotype, we confirmed that decreased level predicts GRN mutations, even in presymptomatic carriers more than four decades before disease onset. We also provided first evidence for the stability of levels throughout longitudinal trajectory in carriers, over a 4-year time span. Finally, we confirmed that progranulin levels constitute a reliable, cost-effective marker, suitable as a screening tool in patients with familial frontotemporal degeneration, and more broadly in patients without family history or with atypical presentations who are less likely to be referred for molecular diagnosis. • Plasma progranulin levels were analyzed in 293 GRN carriers and controls. • Progranulin levels were stable in carriers and controls over a 4-year time span. • Plasma progranulin did not correlate with age at onset and FTD phenotypes. • Different thresholds were suggested for male and female carriers. [ABSTRACT FROM AUTHOR]
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- 2020
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234. Clinical manifestations of intermediate allele carriers in Huntington disease
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Cubo E., Ramos-Arroyo M. A., Martinez-Horta S., Martinez-Descalls A., Calvo S., Gil-Polo CAnne-Catherine Bachoud-Lévi, Anna Rita Bentivoglio, Ida Biunno, Raphael M Bonelli, Jean-Marc Burgunder, Stephen B Dunnett, Joaquim J Ferreira, Olivia J Handley, Arvid Heiberg, Torsten Illmann, G Bernhard Landwehrmeyer, Jamie Levey, Maria Ramos-Arroyo, Jørgen E Nielsen, Susana Pro Koivisto, Markku Päivärinta, Raymund A C Roos, Ana Rojo Sebastián, Sarah J Tabrizi, Wim Vandenberghe, Christine Verellen-Dumoulin, Tereza Uhrova, Jan Wahlström, Jacek Zaremba, Verena Baake, Katrin Barth, Adrien Come, Leonor Correia Guedes, Ana Maria Finisterra, Monica Bascuñana Garde, Reineke Bos, Sabrina Betz, Jenny Callaghan, Selene Capodarca, Sébastien Charpentier, Wildson Vieira da Silva, Martina Di Renzo, Daniel Ecker, Ruth Fullam, Camille Genoves, Mette Gilling, Carina Hvalstedt, Christine Held, Andrea Horta-Barba, Kerstin Koppers, Claudia Lamanna, Matilde Laurà, Asunción Martínez Descals, Saul Martinez-Horta, Tiago Mestre, Sara Minster, Daniela Monza, Lisanne Mütze, Martin Oehmen, Helene Padieu, Laurent Paterski, Nadia Peppa, Beate Rindal, Dawn Rogers, Niini Røren, Pavla Šašinková, Yuri Seliverstov, Catherine Taylor, Erika Timewell, Jenny Townhill, Patricia Trigo Cubillo, Marleen R van Walsem, Marie-Noelle Witjes-Ané, Grzegorz Witkowski, Abigail Wright, Elizaveta Yudina, Daniel Zielonka, Eugeniusz Zielonka, Paola Zinzi, Cécile Minet, Pascale Ribaï, Dominique Van Paemel, Lena Hjermind, Oda Jacobsen, Suzanne Lindquist, Jørgen Nielsen, Lisbeth Regeur, Jette Stockholm, Ida Unmack Larsen, Christina Vangsted-Hansen, Tua Vinther-Jensen, Pia Eklund, Heli Hiivola, Hannele Hypponen, Kirsti Martikainen, Katri Tuuha, Philippe Allain, Dominique Bonneau Marie Bost, Bénédicte Gohier, Marie-Anne Guérid, Audrey Olivier, Julie Prouzet, Adriana Prundean, Clarisse Scherer-Gagou, Christophe Verny, Blandine Babiloni, Sabrina Debruxelles, Charlotte Duché, Cyril Goizet, Laetitia Jameau, Danielle Lafoucrière, Umberto Spampinato, Anne-Catherine Bachoud-Lévi, Farideh Badei, Lotfi Boudali, Catherine Bourdet, Laurent Cléret, Maryline Couette, Cécile Focseneanu, Laurie Lemoine, Graça Morgado, Mehdi Sebaiti, Claire Thiriez, Laetitia Vervoitte, Katia Youssov, Jean-Philippe Azulay, Christelle Chabot, Marie Delfini, Alexandre Eusebio, Frédérique Fluchere, Christine Garreau, Aicha Ghenam, Hélène Grosjean, Laura Mundler, Marielle Nowak, Roland Raseta, Maïté Bertrand, Fabienne Calvas, Samia Cheriet, Laurent Marquine, Michèle Pierre, Jérémie Pariente, Sandrine Rolland, Alice Seris, Valérie Vaquie, Christoph Michael Kosinski, Eva Milkereit, Daniela Probst, Kathrin Reetz, Christian Sass, Johannes Schiefer, Christiane Schlangen, Cornelius J Werner, Gisa Ellrichmann, Lennard Herrmann, Rainer Hoffmann, Barbara Kaminski, Carsten Saft, Kai Boelmans, Christos Ganos, Ines Goerendt, Walburgis Heinicke, Ute Hidding, Jan Lewerenz, Alexander Münchau, Michael Orth, Jenny Schmalfeld, Lars Stubbe, Simone Zittel, Gabriele Diercks, Dirk Dressler, Flverly Francis, Sabine Gayde-Stephan, Heike Gorzolla, Bianca Kramer, Rebecca Minschke, Christoph Schrader, Pawel Tacik, Natalie Bechtel, Heike Beckmann, Stefan Bohlen, Nicole Göpfert, Eva Hölzner, Herwig Lange, Ralf Reilmann, Stefanie Rohm, Silke Rumpf, Sigrun Schepers, Nathalia Weber, Michael Bachmeier, Matthias Dose, Nina Hofstetter, Ralf Marquard, Alzbeta Mühlbäck, Andrea Buck, Julia Connemann, Carolin Geitner, Andrea Kesse, Bernhard Landwehrmeyer, Franziska Lezius, Solveig Nepper, Anke Niess, Ariane Schneider, Daniela Schwenk, Sigurd Süssmuth, Sonja Trautmann, Patrick Weydt, Stephan Klebe, Thomas Musacchio, Christine Leypold, Kerstin Nöth, Claudia Cormio, Marina de Tommaso, Anna Rita Dellomonaco, Olimpia Difruscolo, Giovanni Franco, Vittorio Sciruicchio, Claudia Serpino, Michela Figorilli, Francesco Marrosu, Antonella Muroni, Valeria Piras, Melisa Vacca, Caterina Bartoli, Elisabetta Bertini, Fernanda Fortunato, Elena Ghelli, Andrea Ginestroni, Claudia Mechi, Marco Paganini, Silvia Piacentini, Silvia Pradella, Anna Maria Romoli, Sandro Sorbi, Giuseppe De Michele, Luigi Di Maio, Carlo Rinaldi, Marco Massarelli, Silvio Peluso, Alessandro Roca, Cinzia Valeria Russo, Pierpaolo Sorrentino, Elena Salvatore, Tecla Tucci, Milena Cannella, Valentina Codella, Francesca De Gregorio, Annunziata De Nicola, Francesca Elifani, Tiziana Martino, Francesca Lovo, Irene Mazzante, Martina Petrollini, Maria Simonelli, Ferdinando Squitieri, Maurizio Vezza, Barbara D'Alessio, Chiara Esposito, Giulia Coarelli, Michela Ferraldeschi, Marina Frontali, Gioia Jacopini, Giovanni Ristori, Silvia Romano, Monique S E van Hout, Jeroen P P van Vugt, A Marit de Weert, Marloes Verhoeven, Simon J A van den Bogaard, Eve M Dumas, Ellen P 't Hart, Milou Jacobs, Anne Kampstra, Anne Schoonderbeek, Nils Olav Aanonsen, Olaf Aaserud, Liv Barnett, Kathrine Bjørgo, Nancy Borgerød, Elisabeth Dramstad, Madeleine Fannemel, Jan Frich, Helen Gundersen, Per Gørvell, Kathrine Haggag, Cecilie Haggag Johannessen, Lars Retterstøl, Oddveig Rosby, Jutta Rummel, Alma Sikiric, Olga Solberg, Marleen van Walsem, Ragnhild Wehus, Artur Dziadkiewicz, Agnieszka Konkel, Ewa Narożańska, Malgorzata Nowak, Piotr Robowski, Emilia Sitek, Jaroslaw Slawek, Witold Soltan, Michal Szinwelski, Michał Arkuszewski, Magdalena Błaszczyk, Magdalena Boczarska-Jedynak, Ewelina Ciach-Wysocka, Agnieszka Gorzkowska, Barbara Jasińska-Myga, Aleksandra Kaczmarczyk, Gabriela Kłodowska-Duda, Grzegorz Opala, Monika Rudzińska, Daniel Stompel, Krzysztof Banaszkiewicz, Dorota Boćwińska, Kamila Bojakowska-Jaremek, Małgorzata Dec, Natalia Grabska, Malgorzata Krawczyk, Ewelina Kubowicz, Michalina Malec-Litwinowicz, Agata Stenwak, Andrzej Szczudlik, Elżbieta Szczygieł, Magdalena Wójcik, Anna Wasielewska, Jacek Anioła Anna Bryl, Anna Ciesielska, Aneta Klimberg, Jerzy Marcinkowski, Husam Samara, Justyna Sempołowicz, Bartłomiej Wiśniewski, Anna Gogol, Piotr Janik, Zygmunt Jamrozik, Anna Kaminska, Hubert Kwiecinski, Jakub Antczak, Katarzyna Jachinska, Wioletta Krysa, Maryla Rakowicz, Przemyslaw Richter, Rafal Rola, Danuta Ryglewicz, Halina Sienkiewicz-Jarosz, Iwona Stępniak, Anna Sułek, Elzbieta Zdzienicka, Karolina Ziora-Jakutowicz, Cristina Januário, Filipa Júlio, Ana Salgueiro, Miguel Coelho, Tiago Mendes, Mário Miguel Rosa, Anabela Valadas, Cristina Semedo, Ana Calado, Joana Morgado, Margarida Dias, Manuel Almeida, Carmen Durán Herrera, Patrocinio Garcia Moreno, Jordi Bas, Núria Busquets, Matilde Calopa, Serge Jaumà Classen, Nadia Rodríguez Dedichá, Miquel Aguilar Barbera, Sonia Arribas Pardo, Dolors Badenes Guia, Noemi Calzado, Laura Casas Hernanz, Juan Pablo Tartari Díaz-Zorita, Judit López Catena, Pilar Quiléz Ferrer, Gemma Tome Carruesco, Misericordia Floriach Robert, Cèlia Mareca Viladrich, Elvira Roca, Jesús Miguel Ruiz Idiago, Antonio Villa Riballo, Antonia Campolongo, Ramon Fernandez de Bobadilla, Jaime Kulisevsky Bojarsky, Javier Pagonabarraga, Jesus Perez Perez, Carolina Villa, Maria Angeles Acera Gil, Koldo Berganzo Corrales, Juan Carlos Gomez Esteban, Amaia González, Beatriz Tijero Merino, Esther Cubo, Natividad Mariscal, Sandra Gutierrez Romero, José Matías Arbelo, Rocío Malo de Molina, Idaira Martín, Juan Manuel Periañez, Beatriz Udaeta, Fernando Alonso-Frech, Belén Frades, Marina Ávila Villanueva, Maria Ascension Zea Sevilla, Fernando Alonso Frech, María Del Mar Fenollar, Rocío García-Ramos García, Clara Villanueva, Mónica Bascuñana, Marta Fatás Ventura, Juan García Caldentey, Guillermo García Ribas, Justo García de Yébenes, José Luis López-Sendón Moreno, Verónica Mañanes Barral, Cici Feliz Feliz, Pedro José García Ruíz, Ana García, Rosa Guerrero López, Antonio Herranz Bárcenas, Asunción Martínez-Descals, Angel Martínez Pueyo, Veronica Puertas Martin, Noelia Rodríguez Martínez, María José Sainz Artiga, Vicenta Sánchez, Javier Del Val Fernandez, Carmen Antúnez Almagro, Salvadora Manzanares, Juan Marín Muñoz, María Martirio Antequera Torres, Fuensanta Noguera Perea, Laura Vivancos Moreau, Sonia González, Luis Menéndez Guisasola, Carlos Salvador, René Ribacoba, Pablo Sánchez Lozano, Marta Para Prieto, Aránzazu Gorospe, Inés Legarda Ramirez, Penelope Navas Arques, Monica Rodriguez Lopera, Barbara Vives Pastor, Itziar Gaston, Maria Antonia Ramos-Arroyo, Maria Dolores Martinez-Jaurrieta, José Manuel García Moreno, Carolina Mendez Lucena, José Chacón Peña, Fátima Damas Hermoso, Eva Pacheco Cortegana, Luis Redondo, Cristina Melgar Fernandez, Maite Paredes Mata, Maria Dolores Romero Lemos, Maria Bosca, Juan Andres Burguera, Francisco Castera Brugada Carmen Peiró Vilaplana, Elena Bellosta Diago, Javier López Del Val, Laura Martinez Martinez, Elena López, Peter Berglund, Radu Constantinescu, Gunnel Fredlund, Ulrika Høsterey-Ugander, Liselotte Neleborn-Lingefjärd, Yanik Stebler, Alain Kaelin, Irene Romero, Michael Schüpbach, Sabine Weber Zaugg, Lorna Downie, Roisin Jack, Kirsty Matheson, Zosia Miedzybrodzka, Daniela Rae, Sheila A Simpson, Fiona Summers, Alexandra Ure, Vivien Vaughn, Shahbana Akhtar, Jenny Crooks, Adrienne Curtis, Jenny de Souza, John Piedad, Hugh Rickards, Jan Wright, Elizabeth Coulthard, Louise Gethin, Beverley Hayward, Kasia Sieradzan, Monica Busse, Cynthia Butcher, Stephen Dunnett, Catherine Clenaghan, Sarah Hunt, Lesley Jones, Una Jones, Hanan Khalil, Michael Owen, Kathleen Price, Anne Rosser, Peter Brockie, Jillian Foster, Nicola Johns, Sue McKenzie, Jean Rothery, Gareth Thomas, Shona Yates, Alyson Andrew, Julie Frost, Rupert Noad, Jeremy Cosgrove, Deena Gallantree, Stephanie Hamer, Emma Hobson, Stuart Jamieson, Alison Kraus, Mandy Longthorpe, Ivana Markova, Hannah Musgrave, Caroline Peacy, Ashok Raman, Liz Rowett, Jean Toscano, Sue Wild, Carole Clayton, Pam Yardumian, Heather Dipple, Dawn Freire- Patino, Caroline Hallam, Julia Middleton, Uruj Anjum, Jan Coebergh, Charlotte Eddy, Nayana Lahiri, Meriel McEntagart, Michael Patton, Maria Peterson, Sarah Rose, Thomasin Andrews, Stefanie Brown, Stefania Bruno, Elvina Chu, Karen Doherty, Charlotte Golding, Salman Haider, Davina Hensman, Monica Lewis, Marianne Novak, Aakta Patel, Joy Read, Nicola Robertson, Elisabeth Rosser, Sarah Tabrizi, Rachel Taylor, Thomas Warner, Edward Wild, Natalie Arran, Judith Bek, David Craufurd, Marianne Hare, Liz Howard, Susan Huson, Liz Johnson, Mary Jones, Ashok Krishnamoorthy, Helen Murphy, Emma Oughton, Lucy Partington-Jones, Andrea Sollom, Julie Snowden, Cheryl Stopford, Jennifer Thompson, Iris Trender-Gerhard, Nichola Verstraelen, Leann Westmoreland, Ginette Cass, Lynn Davidson, Jill Davison, Neil Fullerton, Katrina Holmes, Suresh Komati, Sharon McDonnell, Zeid Mohammed, Karen Morgan, Lois Savage, Baldev Singh, Josh Wood, Andrea H Nemeth, Gill Siuda, Ruth Valentine, Kathryn Dixon, Richard Armstrong, David Harrison, Max Hughes, Sandra Large, John O Donovan, Amy Palmer, Andrew Parkinson, Beverley Soltysiak, Leanne Timings, Josh Williams, Oliver Bandmann, Alyson Bradbury, Helen Fairtlough, Kay Fillingham, Isabella Foustanos, Paul Gill, Mbombe Kazoka, Kirsty O'Donovan, Louise Nevitt, Oliver Quarrell, Cat Taylor, Katherine Tidswell, Lesley Gowers, Kingsley Powell, Pamela Bethwaite, Rachel Edwards, Kathleen Fuller, Michelle Phillips, Univ Angers, Okina, E., Cubo, M. A., Ramos-Arroyo, S., Martinez-Horta, A., Martinez-Descall, S., Calvo, CAnne-Catherine Bachoud-Lévi, Gil-Polo, Rita Bentivoglio, Anna, Biunno, Ida, M Bonelli, Raphael, Burgunder, Jean-Marc, B Dunnett, Stephen, J Ferreira, Joaquim, J Handley, Olivia, Heiberg, Arvid, Illmann, Torsten, Bernhard Landwehrmeyer, G, Levey, Jamie, Ramos-Arroyo, Maria, E Nielsen, Jørgen, Pro Koivisto, Susana, Päivärinta, Markku, C Roos, Raymund A, Rojo Sebastián, Ana, J Tabrizi, Sarah, Vandenberghe, Wim, Verellen-Dumoulin, Christine, Uhrova, Tereza, Wahlström, Jan, Zaremba, Jacek, Baake, Verena, Barth, Katrin, Come, Adrien, Correia Guedes, Leonor, Maria Finisterra, Ana, Bascuñana Garde, Monica, Bos, Reineke, Betz, Sabrina, Callaghan, Jenny, Capodarca, Selene, Charpentier, Sébastien, Vieira da Silva, Wildson, Di Renzo, Martina, Ecker, Daniel, Fullam, Ruth, Genoves, Camille, Gilling, Mette, Hvalstedt, Carina, Held, Christine, Horta-Barba, Andrea, Koppers, Kerstin, Lamanna, Claudia, Laurà, Matilde, Martínez Descals, Asunción, Martinez-Horta, Saul, Mestre, Tiago, Minster, Sara, Monza, Daniela, Mütze, Lisanne, Oehmen, Martin, Padieu, Helene, Paterski, Laurent, Peppa, Nadia, Rindal, Beate, Rogers, Dawn, Røren, Niini, Šašinková, Pavla, Seliverstov, Yuri, Taylor, Catherine, Timewell, Erika, Townhill, Jenny, Trigo Cubillo, Patricia, R van Walsem, Marleen, Witjes-Ané, Marie-Noelle, Witkowski, Grzegorz, Wright, Abigail, Yudina, Elizaveta, Zielonka, Daniel, Zielonka, Eugeniusz, Zinzi, Paola, Minet, Cécile, Ribaï, Pascale, Van Paemel, Dominique, Hjermind, Lena, Jacobsen, Oda, Lindquist, Suzanne, Nielsen, Jørgen, Regeur, Lisbeth, Stockholm, Jette, Unmack Larsen, Ida, Vangsted-Hansen, Christina, Vinther-Jensen, Tua, Eklund, Pia, Hiivola, Heli, Hypponen, Hannele, Martikainen, Kirsti, Tuuha, Katri, Allain, Philippe, Bonneau Marie Bost, Dominique, Gohier, Bénédicte, Guérid, Marie-Anne, Olivier, Audrey, Prouzet, Julie, Prundean, Adriana, Scherer-Gagou, Clarisse, Verny, Christophe, Babiloni, Blandine, Debruxelles, Sabrina, Duché, Charlotte, Goizet, Cyril, Jameau, Laetitia, Lafoucrière, Danielle, Spampinato, Umberto, Bachoud-Lévi, Anne-Catherine, Badei, Farideh, Boudali, Lotfi, Bourdet, Catherine, Cléret, Laurent, Couette, Maryline, Focseneanu, Cécile, Lemoine, Laurie, Morgado, Graça, Sebaiti, Mehdi, Thiriez, Claire, Vervoitte, Laetitia, Youssov, Katia, Azulay, Jean-Philippe, Chabot, Christelle, Delfini, Marie, Eusebio, Alexandre, Fluchere, Frédérique, Garreau, Christine, Ghenam, Aicha, Grosjean, Hélène, Mundler, Laura, Nowak, Marielle, Raseta, Roland, Bertrand, Maïté, Calvas, Fabienne, Cheriet, Samia, Marquine, Laurent, Pierre, Michèle, Pariente, Jérémie, Rolland, Sandrine, Seris, Alice, Vaquie, Valérie, Michael Kosinski, Christoph, Milkereit, Eva, Probst, Daniela, Reetz, Kathrin, Sass, Christian, Schiefer, Johanne, Schlangen, Christiane, J Werner, Corneliu, Ellrichmann, Gisa, Herrmann, Lennard, Hoffmann, Rainer, Kaminski, Barbara, Saft, Carsten, Boelmans, Kai, Ganos, Christo, Goerendt, Ine, Heinicke, Walburgi, Hidding, Ute, Lewerenz, Jan, Münchau, Alexander, Orth, Michael, Schmalfeld, Jenny, Stubbe, Lar, Zittel, Simone, Diercks, Gabriele, Dressler, Dirk, Francis, Flverly, Gayde-Stephan, Sabine, Gorzolla, Heike, Kramer, Bianca, Minschke, Rebecca, Schrader, Christoph, Tacik, Pawel, Bechtel, Natalie, Beckmann, Heike, Bohlen, Stefan, Göpfert, Nicole, Hölzner, Eva, Lange, Herwig, Reilmann, Ralf, Rohm, Stefanie, Rumpf, Silke, Schepers, Sigrun, Weber, Nathalia, Bachmeier, Michael, Dose, Matthia, Hofstetter, Nina, Marquard, Ralf, Mühlbäck, Alzbeta, Buck, Andrea, Connemann, Julia, Geitner, Carolin, Kesse, Andrea, Landwehrmeyer, Bernhard, Lezius, Franziska, Nepper, Solveig, Niess, Anke, Schneider, Ariane, Schwenk, Daniela, Süssmuth, Sigurd, Trautmann, Sonja, Weydt, Patrick, Klebe, Stephan, Musacchio, Thoma, Leypold, Christine, Nöth, Kerstin, Cormio, Claudia, de Tommaso, Marina, Rita Dellomonaco, Anna, Difruscolo, Olimpia, Franco, Giovanni, Sciruicchio, Vittorio, Serpino, Claudia, Figorilli, Michela, Marrosu, Francesco, Muroni, Antonella, Piras, Valeria, Vacca, Melisa, Bartoli, Caterina, Bertini, Elisabetta, Fortunato, Fernanda, Ghelli, Elena, Ginestroni, Andrea, Mechi, Claudia, Paganini, Marco, Piacentini, Silvia, Pradella, Silvia, Maria Romoli, Anna, Sorbi, Sandro, DE MICHELE, Giuseppe, Di Maio, Luigi, Rinaldi, Carlo, Massarelli, Marco, Peluso, Silvio, Roca, Alessandro, Russo, CINZIA VALERIA, Sorrentino, Pierpaolo, Salvatore, Elena, Tucci, Tecla, Cannella, Milena, Codella, Valentina, De Gregorio, Francesca, De Nicola, Annunziata, Elifani, Francesca, Martino, Tiziana, Lovo, Francesca, Mazzante, Irene, Petrollini, Martina, Simonelli, Maria, Squitieri, Ferdinando, Vezza, Maurizio, D'Alessio, Barbara, Esposito, Chiara, Coarelli, Giulia, Ferraldeschi, Michela, Frontali, Marina, Jacopini, Gioia, Ristori, Giovanni, Romano, Silvia, E van Hout, Monique S, P van Vugt, Jeroen P, Marit de Weert, A, Verhoeven, Marloe, A van den Bogaard, Simon J, M Dumas, Eve, P 't Hart, Ellen, Jacobs, Milou, Kampstra, Anne, Schoonderbeek, Anne, Olav Aanonsen, Nil, Aaserud, Olaf, Barnett, Liv, Bjørgo, Kathrine, Borgerød, Nancy, Dramstad, Elisabeth, Fannemel, Madeleine, Frich, Jan, Gundersen, Helen, Gørvell, Per, Haggag, Kathrine, Haggag Johannessen, Cecilie, Retterstøl, Lar, Rosby, Oddveig, Rummel, Jutta, Sikiric, Alma, Solberg, Olga, van Walsem, Marleen, Wehus, Ragnhild, Dziadkiewicz, Artur, Konkel, Agnieszka, Narożańska, Ewa, Nowak, Malgorzata, Robowski, Piotr, Sitek, Emilia, Slawek, Jaroslaw, Soltan, Witold, Szinwelski, Michal, Arkuszewski, Michał, Błaszczyk, Magdalena, Boczarska-Jedynak, Magdalena, Ciach-Wysocka, Ewelina, Gorzkowska, Agnieszka, Jasińska-Myga, Barbara, Kaczmarczyk, Aleksandra, Kłodowska-Duda, Gabriela, Opala, Grzegorz, Rudzińska, Monika, Stompel, Daniel, Banaszkiewicz, Krzysztof, Boćwińska, Dorota, Bojakowska-Jaremek, Kamila, Dec, Małgorzata, Grabska, Natalia, Krawczyk, Malgorzata, Kubowicz, Ewelina, Malec-Litwinowicz, Michalina, Stenwak, Agata, Szczudlik, Andrzej, Szczygieł, Elżbieta, Wójcik, Magdalena, Wasielewska, Anna, Anioła Anna Bryl, Jacek, Ciesielska, Anna, Klimberg, Aneta, Marcinkowski, Jerzy, Samara, Husam, Sempołowicz, Justyna, Wiśniewski, Bartłomiej, Gogol, Anna, Janik, Piotr, Jamrozik, Zygmunt, Kaminska, Anna, Kwiecinski, Hubert, Antczak, Jakub, Jachinska, Katarzyna, Krysa, Wioletta, Rakowicz, Maryla, Richter, Przemyslaw, Rola, Rafal, Ryglewicz, Danuta, Sienkiewicz-Jarosz, Halina, Stępniak, Iwona, Sułek, Anna, Zdzienicka, Elzbieta, Ziora-Jakutowicz, Karolina, Januário, Cristina, Júlio, Filipa, Salgueiro, Ana, Coelho, Miguel, Mendes, Tiago, Miguel Rosa, Mário, Valadas, Anabela, Semedo, Cristina, Calado, Ana, Morgado, Joana, Dias, Margarida, Almeida, Manuel, Durán Herrera, Carmen, Garcia Moreno, Patrocinio, Bas, Jordi, Busquets, Núria, Calopa, Matilde, Jaumà Classen, Serge, Rodríguez Dedichá, Nadia, Aguilar Barbera, Miquel, Arribas Pardo, Sonia, Badenes Guia, Dolor, Calzado, Noemi, Casas Hernanz, Laura, Pablo Tartari Díaz-Zorita, Juan, López Catena, Judit, Quiléz Ferrer, Pilar, Tome Carruesco, Gemma, Floriach Robert, Misericordia, Mareca Viladrich, Cèlia, Roca, Elvira, Miguel Ruiz Idiago, Jesú, Villa Riballo, Antonio, Campolongo, Antonia, Fernandez de Bobadilla, Ramon, Kulisevsky Bojarsky, Jaime, Pagonabarraga, Javier, Perez Perez, Jesu, Villa, Carolina, Angeles Acera Gil, Maria, Berganzo Corrales, Koldo, Carlos Gomez Esteban, Juan, González, Amaia, Tijero Merino, Beatriz, Cubo, Esther, Mariscal, Natividad, Gutierrez Romero, Sandra, Matías Arbelo, José, Malo de Molina, Rocío, Martín, Idaira, Manuel Periañez, Juan, Udaeta, Beatriz, Alonso-Frech, Fernando, Frades, Belén, Ávila Villanueva, Marina, Ascension Zea Sevilla, Maria, Alonso Frech, Fernando, Del Mar Fenollar, María, García-Ramos García, Rocío, Villanueva, Clara, Bascuñana, Mónica, Fatás Ventura, Marta, García Caldentey, Juan, García Ribas, Guillermo, García de Yébenes, Justo, Luis López-Sendón Moreno, José, Mañanes Barral, Verónica, Feliz Feliz, Cici, José García Ruíz, Pedro, García, Ana, Guerrero López, Rosa, Herranz Bárcenas, Antonio, Martínez-Descals, Asunción, Martínez Pueyo, Angel, Puertas Martin, Veronica, Rodríguez Martínez, Noelia, José Sainz Artiga, María, Sánchez, Vicenta, Del Val Fernandez, Javier, Antúnez Almagro, Carmen, Manzanares, Salvadora, Marín Muñoz, Juan, Martirio Antequera Torres, María, Noguera Perea, Fuensanta, Vivancos Moreau, Laura, González, Sonia, Menéndez Guisasola, Lui, Salvador, Carlo, Ribacoba, René, Sánchez Lozano, Pablo, Para Prieto, Marta, Gorospe, Aránzazu, Legarda Ramirez, Iné, Navas Arques, Penelope, Rodriguez Lopera, Monica, Vives Pastor, Barbara, Gaston, Itziar, Antonia Ramos-Arroyo, Maria, Dolores Martinez-Jaurrieta, Maria, Manuel García Moreno, José, Mendez Lucena, Carolina, Chacón Peña, José, Damas Hermoso, Fátima, Pacheco Cortegana, Eva, Redondo, Lui, Melgar Fernandez, Cristina, Paredes Mata, Maite, Dolores Romero Lemos, Maria, Bosca, Maria, Andres Burguera, Juan, Castera Brugada Carmen Peiró Vilaplana, Francisco, Bellosta Diago, Elena, López Del Val, Javier, Martinez Martinez, Laura, López, Elena, Berglund, Peter, Constantinescu, Radu, Fredlund, Gunnel, Høsterey-Ugander, Ulrika, Neleborn-Lingefjärd, Liselotte, Stebler, Yanik, Kaelin, Alain, Romero, Irene, Schüpbach, Michael, Weber Zaugg, Sabine, Downie, Lorna, Jack, Roisin, Matheson, Kirsty, Miedzybrodzka, Zosia, Rae, Daniela, A Simpson, Sheila, Summers, Fiona, Ure, Alexandra, Vaughn, Vivien, Akhtar, Shahbana, Crooks, Jenny, Curtis, Adrienne, de Souza, Jenny, Piedad, John, Rickards, Hugh, Wright, Jan, Coulthard, Elizabeth, Gethin, Louise, Hayward, Beverley, Sieradzan, Kasia, Busse, Monica, Butcher, Cynthia, Dunnett, Stephen, Clenaghan, Catherine, Hunt, Sarah, Jones, Lesley, Jones, Una, Khalil, Hanan, Owen, Michael, Price, Kathleen, Rosser, Anne, Brockie, Peter, Foster, Jillian, Johns, Nicola, Mckenzie, Sue, Rothery, Jean, Thomas, Gareth, Yates, Shona, Andrew, Alyson, Frost, Julie, Noad, Rupert, Cosgrove, Jeremy, Gallantree, Deena, Hamer, Stephanie, Hobson, Emma, Jamieson, Stuart, Kraus, Alison, Longthorpe, Mandy, Markova, Ivana, Musgrave, Hannah, Peacy, Caroline, Raman, Ashok, Rowett, Liz, Toscano, Jean, Wild, Sue, Clayton, Carole, Yardumian, Pam, Dipple, Heather, Freire- Patino, Dawn, Hallam, Caroline, Middleton, Julia, Anjum, Uruj, Coebergh, Jan, Eddy, Charlotte, Lahiri, Nayana, Mcentagart, Meriel, Patton, Michael, Peterson, Maria, Rose, Sarah, Andrews, Thomasin, Brown, Stefanie, Bruno, Stefania, Chu, Elvina, Doherty, Karen, Golding, Charlotte, Haider, Salman, Hensman, Davina, Lewis, Monica, Novak, Marianne, Patel, Aakta, Read, Joy, Robertson, Nicola, Rosser, Elisabeth, Tabrizi, Sarah, Taylor, Rachel, Warner, Thoma, Wild, Edward, Arran, Natalie, Bek, Judith, Craufurd, David, Hare, Marianne, Howard, Liz, Huson, Susan, Johnson, Liz, Jones, Mary, Krishnamoorthy, Ashok, Murphy, Helen, Oughton, Emma, Partington-Jones, Lucy, Sollom, Andrea, Snowden, Julie, Stopford, Cheryl, Thompson, Jennifer, Trender-Gerhard, Iri, Verstraelen, Nichola, Westmoreland, Leann, Cass, Ginette, Davidson, Lynn, Davison, Jill, Fullerton, Neil, Holmes, Katrina, Komati, Suresh, Mcdonnell, Sharon, Mohammed, Zeid, Morgan, Karen, Savage, Loi, Singh, Baldev, Wood, Josh, H Nemeth, Andrea, Siuda, Gill, Valentine, Ruth, Dixon, Kathryn, Armstrong, Richard, Harrison, David, Hughes, Max, Large, Sandra, O Donovan, John, Palmer, Amy, Parkinson, Andrew, Soltysiak, Beverley, Timings, Leanne, Williams, Josh, Bandmann, Oliver, Bradbury, Alyson, Fairtlough, Helen, Fillingham, Kay, Foustanos, Isabella, Gill, Paul, Kazoka, Mbombe, O'Donovan, Kirsty, Nevitt, Louise, Quarrell, Oliver, Taylor, Cat, Tidswell, Katherine, Gowers, Lesley, Powell, Kingsley, Bethwaite, Pamela, Edwards, Rachel, Fuller, Kathleen, Phillips, Michelle, Cubo, E., Ramos-Arroyo, M. A., Martinez-Horta, S., Martinez-Descalls, A., Russo, C. V., Calvo, S., Gil-Polo, C., Biologie Neurovasculaire et Mitochondriale Intégrée (BNMI), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université d'Angers (UA), Ramos-Arroyo, María A., Martínez-Descalls, Asunción, Calvo, Sara, and Gil-Polo, Cecilia
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0301 basic medicine ,Registrie ,Adult ,Male ,medicine.medical_specialty ,Aging ,Heterozygote ,Genetic counseling ,Motor Disorders ,Disease ,Severity of Illness Index ,03 medical and health sciences ,Cognition Disorder ,0302 clinical medicine ,Trinucleotide Repeats ,Internal medicine ,medicine ,Humans ,Registries ,Allele ,Motor Disorder ,Alleles ,Huntingtin Protein ,[SDV.MHEP] Life Sciences [q-bio]/Human health and pathology ,business.industry ,Medicine (all) ,Trinucleotide Repeat ,Cognition ,Genetic Status ,Middle Aged ,Phenotype ,Europe ,Settore MED/26 - NEUROLOGIA ,030104 developmental biology ,Huntington Disease ,Case-Control Studies ,Cohort ,medicine (all) ,neurology (clinical) ,controlled clinical trial (topic) ,Quality of Life ,Female ,Neurology (clinical) ,business ,Case-Control Studie ,Cognition Disorders ,030217 neurology & neurosurgery ,[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology ,Human - Abstract
International audience; OBJECTIVE: There is controversy about the clinical consequences of intermediate alleles (IAs) in Huntington disease (HD). The main objective of this study was to establish the clinical manifestations of IA carriers for a prospective, international, European HD registry.METHODS: We assessed a cohort of participants at risk with RESULTS: Of 12,190 participants, 657 (5.38%) with CONCLUSIONS: Although aging worsened the UHDRS scores independently of the genetic status, IAs might confer a late-onset abnormal motor and cognitive phenotype. These results might have important implications for genetic counseling.CLINICALTRIALSGOV IDENTIFIER: NCT01590589.
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- 2016
235. Errata
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Chollet, François, Tardy, Jean, Albucher, Jean-François, Thalamas, Claire, Berard, Emilie, Lamy, Catherine, Bejot, Yannick, Deltour, Sandrine, Jaillard, Assia, Niclot, Philippe, Guillon, Benoit, Moulin, Thierry, Marque, Philippe, Pariente, Jérémie, Arnaud, Catherine, and Loubinoux, Isabelle
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CONVALESCENCE , *FLUOXETINE , *LONGITUDINAL method , *MOTOR ability , *STROKE , *RANDOMIZED controlled trials , *TREATMENT effectiveness , *BLIND experiment , *ACUTE diseases , *PHARMACODYNAMICS , *THERAPEUTICS - Abstract
Background: Hemiplegia and hemiparesis are the most common deficits caused by stroke. A few small clinical trials suggest that fluoxetine enhances motor recovery but its clinical efficacy is unknown. We therefore aimed to investigate whether fluoxetine would enhance motor recovery if given soon after an ischaemic stroke to patients who have motor deficits.Methods: In this double-blind, placebo-controlled trial, patients from nine stroke centres in France who had ischaemic stroke and hemiplegia or hemiparesis, had Fugl-Meyer motor scale (FMMS) scores of 55 or less, and were aged between 18 years and 85 years were eligible for inclusion. Patients were randomly assigned, using a computer random-number generator, in a 1:1 ratio to fluoxetine (20 mg once per day, orally) or placebo for 3 months starting 5-10 days after the onset of stroke. All patients had physiotherapy. The primary outcome measure was the change on the FMMS between day 0 and day 90 after the start of the study drug. Participants, carers, and physicians assessing the outcome were masked to group assignment. Analysis was of all patients for whom data were available (full analysis set). This trial is registered with ClinicalTrials.gov, number NCT00657163.Findings: 118 patients were randomly assigned to fluoxetine (n=59) or placebo (n=59), and 113 were included in the analysis (57 in the fluoxetine group and 56 in the placebo group). Two patients died before day 90 and three withdrew from the study. FMMS improvement at day 90 was significantly greater in the fluoxetine group (adjusted mean 34·0 points [95% CI 29·7-38·4]) than in the placebo group (24·3 points [19·9-28·7]; p=0·003). The main adverse events in the fluoxetine and placebo groups were hyponatraemia (two [4%] vs two [4%]), transient digestive disorders including nausea, diarrhoea, and abdominal pain (14 [25%] vs six [11%]), hepatic enzyme disorders (five [9%] vs ten [18%]), psychiatric disorders (three [5%] vs four [7%]), insomnia (19 [33%] vs 20 [36%]), and partial seizure (one [<1%] vs 0).Interpretation: In patients with ischaemic stroke and moderate to severe motor deficit, the early prescription of fluoxetine with physiotherapy enhanced motor recovery after 3 months. Modulation of spontaneous brain plasticity by drugs is a promising pathway for treatment of patients with ischaemic stroke and moderate to severe motor deficit.Funding: Public French National Programme for Clinical Research. [ABSTRACT FROM AUTHOR]- Published
- 2011
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236. Cerebral Amyloid Angiopathy-Related Inflammation and Biopsy-Positive Primary Angiitis of the CNS: A Comparative Study.
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Grangeon L, Boulouis G, Capron J, Bala F, Renard D, Raposo N, Ozkul-Wermester O, Triquenot-Bagan A, Ayrignac X, Wallon D, Gerardin E, Kerschen P, Sablot D, Formaglio M, Pico F, Turc G, Verny M, Humbertjean L, Gaudron M, Vannier S, Dequatre N, Guillon B, Isabel C, Arquizan C, Detante O, Godard S, Casolla B, Levraut M, Gollion C, Gerfaud-Valentin M, Kremer L, Daelman L, Lambert N, Lanthier S, Poppe A, Régent A, Weisenburger-Lile D, Verdure P, Quesney G, Vautier M, Wacongne A, Thouvenot E, Pariente J, Coulette S, Labauge PM, Olivier N, Allou T, Zephir H, Néel A, Bresch S, Terrier B, Martinaud O, Schneckenburger R, Papo T, Comarmond-Ortoli C, Jouvent E, Subréville M, Poncet-Megemont L, Khatib MA, Lun F, Henry C, Magnin E, Thomas Q, Graber M, Boukriche Y, Blanchet-Fourcade G, Ratiu D, Pagnoux C, Touzé E, de Boysson H, Alamowitch S, and Nehme A
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- Humans, Female, Male, Aged, Middle Aged, Retrospective Studies, Biopsy, Magnetic Resonance Imaging, Aged, 80 and over, Brain pathology, Brain diagnostic imaging, Adult, Recurrence, Cerebral Amyloid Angiopathy diagnostic imaging, Cerebral Amyloid Angiopathy pathology, Cerebral Amyloid Angiopathy complications, Vasculitis, Central Nervous System diagnostic imaging, Vasculitis, Central Nervous System pathology
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Background and Objectives: Cerebral amyloid angiopathy-related inflammation (CAA-RI) and biopsy-positive primary angiitis of the CNS (BP-PACNS) have overlapping clinicoradiologic presentations. It is unknown whether clinical and radiologic features can differentiate CAA-RI from BP-PACNS and whether both diseases have different relapse rates. The objectives of this study were to compare clinicoradiologic presentations and relapse rates in patients with CAA-RI vs BP-PACNS., Methods: Patients with CAA-RI and BP-PACNS were enrolled from 2 retrospective multicenter cohorts. Patients with CAA-RI were biopsy-positive or met probable clinicoradiologic criteria. Patients with BP-PACNS had histopathologic confirmation of CNS angiitis, with no secondary etiology. A neuroradiologist read brain MRIs, blinded to the diagnosis of CAA-RI or BP-PACNS. Clinicoradiologic features were compared using univariable logistic regression models. Relapse rates were compared using a univariable Fine-Gray subdistribution hazard model, with death as a competing risk., Results: This study enrolled 104 patients with CAA-RI (mean age 73 years, 48% female sex) and 52 patients with BP-PACNS (mean age 45 years, 48% female sex). Patients with CAA-RI more often had white matter hyperintense lesions meeting the probable CAA-RI criteria (93% vs 51%, p < 0.001), acute subarachnoid hemorrhage (15% vs 2%, p = 0.02), cortical superficial siderosis (27% vs 4%, p < 0.001), ≥1 lobar microbleed (94% vs 26%, p < 0.001), past intracerebral hemorrhage (17% vs 4%, p = 0.04), ≥21 visible centrum semiovale perivascular spaces (34% vs 4%, p < 0.01), and leptomeningeal enhancement (70% vs 27%, p < 0.001). Patients with BP-PACNS more often had headaches (56% vs 31%, p < 0.01), motor deficits (56% vs 36%, p = 0.02), and nonischemic parenchymal gadolinium enhancement (82% vs 16%, p < 0.001). The prevalence of acute ischemic lesions was 18% in CAA-RI and 22% in BP-PACNS ( p = 0.57). The features with the highest specificity for CAA-RI were acute subarachnoid hemorrhage (98%), cortical superficial siderosis (96%), past intracerebral hemorrhage (96%), and ≥21 visible centrum semiovale perivascular spaces (96%). The probable CAA-RI criteria had a 71% sensitivity (95% CI 44%-90%) and 91% specificity (95% CI 79%-98%) in differentiating biopsy-positive CAA-RI from BP-PACNS. The rate of relapse in the first 2 years after remission was lower in CAA-RI than in BP-PACNS (hazard ratio 0.46, 95% CI 0.22-0.96, p = 0.04)., Conclusion: Clinicoradiologic features differed between patients with CAA-RI and those with BP-PACNS. Specific markers for CAA-RI were hemorrhagic signs of subarachnoid involvement, past intracerebral hemorrhage, ≥21 visible centrum semiovale perivascular spaces, and the probable CAA-RI criteria. A biopsy remains necessary for diagnosis in some cases of CAA-RI. The rate of relapse in the first 2 years after disease remission was lower in CAA-RI than in BP-PACNS.
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- 2024
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237. Downstream Biomarker Effects of Gantenerumab or Solanezumab in Dominantly Inherited Alzheimer Disease: The DIAN-TU-001 Randomized Clinical Trial.
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Wagemann O, Liu H, Wang G, Shi X, Bittner T, Scelsi MA, Farlow MR, Clifford DB, Supnet-Bell C, Santacruz AM, Aschenbrenner AJ, Hassenstab JJ, Benzinger TLS, Gordon BA, Coalier KA, Cruchaga C, Ibanez L, Perrin RJ, Xiong C, Li Y, Morris JC, Lah JJ, Berman SB, Roberson ED, van Dyck CH, Galasko D, Gauthier S, Hsiung GR, Brooks WS, Pariente J, Mummery CJ, Day GS, Ringman JM, Mendez PC, St George-Hyslop P, Fox NC, Suzuki K, Okhravi HR, Chhatwal J, Levin J, Jucker M, Sims JR, Holdridge KC, Proctor NK, Yaari R, Andersen SW, Mancini M, Llibre-Guerra J, Bateman RJ, and McDade E
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- Humans, Female, Male, Double-Blind Method, Middle Aged, Adult, Amyloid beta-Peptides cerebrospinal fluid, Chitinase-3-Like Protein 1 blood, Chitinase-3-Like Protein 1 cerebrospinal fluid, Aged, Neurofilament Proteins cerebrospinal fluid, Neurofilament Proteins blood, Antibodies, Monoclonal, Humanized administration & dosage, Antibodies, Monoclonal, Humanized pharmacology, Antibodies, Monoclonal, Humanized therapeutic use, Alzheimer Disease drug therapy, Alzheimer Disease cerebrospinal fluid, Alzheimer Disease blood, Biomarkers cerebrospinal fluid, Biomarkers blood
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Importance: Effects of antiamyloid agents, targeting either fibrillar or soluble monomeric amyloid peptides, on downstream biomarkers in cerebrospinal fluid (CSF) and plasma are largely unknown in dominantly inherited Alzheimer disease (DIAD)., Objective: To investigate longitudinal biomarker changes of synaptic dysfunction, neuroinflammation, and neurodegeneration in individuals with DIAD who are receiving antiamyloid treatment., Design, Setting, and Participants: From 2012 to 2019, the Dominantly Inherited Alzheimer Network Trial Unit (DIAN-TU-001) study, a double-blind, placebo-controlled, randomized clinical trial, investigated gantenerumab and solanezumab in DIAD. Carriers of gene variants were assigned 3:1 to either drug or placebo. The present analysis was conducted from April to June 2023. DIAN-TU-001 spans 25 study sites in 7 countries. Biofluids and neuroimaging from carriers of DIAD gene variants in the gantenerumab, solanezumab, and placebo groups were analyzed., Interventions: In 2016, initial dosing of gantenerumab, 225 mg (subcutaneously every 4 weeks) was increased every 8 weeks up to 1200 mg. In 2017, initial dosing of solanezumab, 400 mg (intravenously every 4 weeks) was increased up to 1600 mg every 4 weeks., Main Outcomes and Measures: Longitudinal changes in CSF levels of neurogranin, soluble triggering receptor expressed on myeloid cells 2 (sTREM2), chitinase 3-like 1 protein (YKL-40), glial fibrillary acidic protein (GFAP), neurofilament light protein (NfL), and plasma levels of GFAP and NfL., Results: Of 236 eligible participants screened, 43 were excluded. A total of 142 participants (mean [SD] age, 44 [10] years; 72 female [51%]) were included in the study (gantenerumab, 52 [37%]; solanezumab, 50 [35%]; placebo, 40 [28%]). Relative to placebo, gantenerumab significantly reduced CSF neurogranin level at year 4 (mean [SD] β = -242.43 [48.04] pg/mL; P < .001); reduced plasma GFAP level at year 1 (mean [SD] β = -0.02 [0.01] ng/mL; P = .02), year 2 (mean [SD] β = -0.03 [0.01] ng/mL; P = .002), and year 4 (mean [SD] β = -0.06 [0.02] ng/mL; P < .001); and increased CSF sTREM2 level at year 2 (mean [SD] β = 1.12 [0.43] ng/mL; P = .01) and year 4 (mean [SD] β = 1.06 [0.52] ng/mL; P = .04). Solanezumab significantly increased CSF NfL (log) at year 4 (mean [SD] β = 0.14 [0.06]; P = .02). Correlation analysis for rates of change found stronger correlations between CSF markers and fluid markers with Pittsburgh compound B positron emission tomography for solanezumab and placebo., Conclusions and Relevance: This randomized clinical trial supports the importance of fibrillar amyloid reduction in multiple AD-related processes of neuroinflammation and neurodegeneration in CSF and plasma in DIAD. Additional studies of antiaggregated amyloid therapies in sporadic AD and DIAD are needed to determine the utility of nonamyloid biomarkers in determining disease modification., Trial Registration: ClinicalTrials.gov Identifier: NCT04623242.
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- 2024
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238. MRI hypoperfusion as a determinant of cognitive impairment in adults with Moyamoya angiopathy.
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Giroud M, Planton M, Darcourt J, Raposo N, Brandicourt P, Mirabel H, Hervé D, Viguier A, Albucher JF, Pariente J, Olivot JM, Bonneville F, Péran P, and Calviere L
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- Humans, Female, Male, Adult, Retrospective Studies, Middle Aged, Cerebrovascular Circulation physiology, Neuropsychological Tests statistics & numerical data, Brain diagnostic imaging, Brain pathology, Brain blood supply, Brain physiopathology, Moyamoya Disease diagnostic imaging, Moyamoya Disease physiopathology, Moyamoya Disease psychology, Moyamoya Disease complications, Moyamoya Disease pathology, Cognitive Dysfunction diagnostic imaging, Cognitive Dysfunction physiopathology, Cognitive Dysfunction etiology, Cognitive Dysfunction pathology, Magnetic Resonance Imaging
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Introduction: In Moyamoya angiopathy (MMA), mechanisms underlying cognitive impairment remain debated. We aimed to assess the association of cognitive impairment with the degree and the topography of cerebral hypoperfusion in MMA., Methods: A retrospective analysis of neuropsychological and perfusion MRI data from adults with MMA was performed. Ischemic and haemorrhagic lesion masks were created to account for cerebral lesions in the analysis of cerebral perfusion. Whole brain volume of hypoperfused parenchyma was outlined on perfusion maps using different Tmax thresholds from 4 to 12 s. Regional analysis produced mean Tmax values at different regions of interest. Analyses compared perfusion ratios in patients with and without cognitive impairment, with multivariable logistic regression analysis to identify predictive factors., Results: Cognitive impairment was found in 20/48 (41.7%) patients. Attention/processing speed and memory were equally impaired (24%) followed by executive domain (23%). After adjustment, especially for lesion volume, hypoperfused parenchyma volume outlined by Tmax > 4 s or Tmax > 5 s thresholds was an independent factor of cognitive impairment (OR for Tmax > 4 s = 1.06 [CI 95% 1.008-1.123]) as well as attention/processing speed (OR for Tmax > 4 s = 1.07 [CI 95% 1.003-1.133]) and executive domains (OR for Tmax > 5 s = 1.08 [CI 95% 1.004-1.158]). Regarding cognitive functions, patients with processing speed and flexibility impairment had higher frontal Tmax compared to other ROIs and to patients with normal test scores., Discussion: Cerebral hypoperfusion emerged as an independent factor of cognitive impairment in MMA particularly in attention/processing speed and executive domains, with a strong contribution of frontal areas., Conclusion: Considering this association, revascularization surgery could improve cognitive impairment., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
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- 2024
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239. Translocator protein (TSPO) genotype does not change cerebrospinal fluid levels of glial activation, axonal and synaptic damage markers in early Alzheimer's disease.
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Gouilly D, Vrillon A, Bertrand E, Goubeaud M, Catala H, Germain J, Ainaoui N, Rafiq M, Nogueira L, Mouton-Liger F, Planton M, Salabert AS, Hitzel A, Méligne D, Jasse L, Sarton B, Silva S, Lemesle B, Péran P, Payoux P, Thalamas C, Paquet C, and Pariente J
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Background: PET imaging of the translocator protein (TSPO) is used to assess in vivo brain inflammation. One of the main methodological issues with this method is the allelic dependence of the radiotracer affinity. In Alzheimer's disease (AD), previous studies have shown similar clinical and patho-biological profiles between TSPO genetic subgroups. However, there is no evidence regarding the effect of the TSPO genotype on cerebrospinal-fluid biomarkers of glial activation, and synaptic and axonal damage., Method: We performed a trans-sectional study in early AD to compare cerebrospinal-fluid levels of GFAP, YKL-40, sTREM2, IL-6, IL-10, NfL and neurogranin between TSPO genetic subgroups., Results: We recruited 33 patients with early AD including 16 (48%) high affinity binders, 13 (39%) mixed affinity binders, and 4/33 (12%) low affinity binders. No difference was observed in terms of demographics, and cerebrospinal fluid levels of each biomarker for the different subgroups., Conclusion: TSPO genotype is not associated with a change in glial activation, synaptic and axonal damage in early AD. Further studies with larger numbers of participants will be needed to confirm that the inclusion of specific TSPO genetic subgroups does not introduce selection bias in studies and trials of AD that combine TSPO imaging with cerebrospinal fluid biomarkers., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dominique Gouilly received research funding from the Fondation de l’Avenir (Paris, France) for this study. Other authors have no relevant financial or non-financial interests to disclose., (Copyright © 2024. Published by Elsevier Inc.)
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- 2024
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240. Assessment of Mendelian and risk-factor genes in Alzheimer disease: A prospective nationwide clinical utility study and recommendations for genetic screening.
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Nicolas G, Zaréa A, Lacour M, Quenez O, Rousseau S, Richard AC, Bonnevalle A, Schramm C, Olaso R, Sandron F, Boland A, Deleuze JF, Andriuta D, Anthony P, Auriacombe S, Balageas AC, Ballan G, Barbay M, Béjot Y, Belliard S, Benaiteau M, Bennys K, Bombois S, Boutoleau-Bretonnière C, Branger P, Carlier J, Cartz-Piver L, Cassagnaud P, Ceccaldi MP, Chauviré V, Chen Y, Cogez J, Cognat E, Contegal-Callier F, Corneille L, Couratier P, Cretin B, Crinquette C, Dauriat B, Dautricourt S, de la Sayette V, de Liège A, Deffond D, Demurger F, Deramecourt V, Derollez C, Dionet E, Doco Fenzy M, Dumurgier J, Dutray A, Etcharry-Bouyx F, Formaglio M, Gabelle A, Gainche-Salmon A, Godefroy O, Graber M, Gregoire C, Grimaldi S, Gueniat J, Gueriot C, Guillet-Pichon V, Haffen S, Hanta CR, Hardy C, Hautecloque G, Heitz C, Hourregue C, Jonveaux T, Jurici S, Koric L, Krolak-Salmon P, Lagarde J, Lanoiselée HM, Laurens B, Le Ber I, Le Guyader G, Leblanc A, Lebouvier T, Levy R, Lippi A, Mackowiak MA, Magnin E, Marelli C, Martinaud O, Maureille A, Migliaccio R, Milongo-Rigal E, Mohr S, Mollion H, Morin A, Nivelle J, Noiray C, Olivieri P, Paquet C, Pariente J, Pasquier F, Perron A, Philippi N, Planche V, Pouclet-Courtemanche H, Rafiq M, Rollin-Sillaire A, Roué-Jagot C, Saracino D, Sarazin M, Sauvée M, Sellal F, Teichmann M, Thauvin C, Thomas Q, Tisserand C, Turpinat C, Van Damme L, Vercruysse O, Villain N, Wagemann N, Charbonnier C, and Wallon D
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- Humans, Female, Male, Aged, Risk Factors, Prospective Studies, Middle Aged, Presenilin-1 genetics, Pedigree, Age of Onset, Amyloid beta-Protein Precursor genetics, Aged, 80 and over, Alzheimer Disease genetics, Alzheimer Disease diagnosis, Genetic Testing methods, Genetic Predisposition to Disease, Exome Sequencing, Presenilin-2 genetics, Membrane Glycoproteins, Receptors, Immunologic
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Purpose: To assess the likely pathogenic/pathogenic (LP/P) variants rates in Mendelian dementia genes and the moderate-to-strong risk factors rates in patients with Alzheimer disease (AD)., Methods: We included 700 patients in a prospective study and performed exome sequencing. A panel of 28 Mendelian and 6 risk-factor genes was interpreted and returned to patients. We built a framework for risk variant interpretation and risk gradation and assessed the detection rates among early-onset AD (EOAD, age of onset (AOO) ≤65 years, n = 608) depending on AOO and pedigree structure and late-onset AD (66 < AOO < 75, n = 92)., Results: Twenty-one patients carried a LP/P variant in a Mendelian gene (all with EOAD, 3.4%), 20 of 21 affected APP, PSEN1, or PSEN2. LP/P variant detection rates in EOAD ranged from 1.7% to 11.6% based on AOO and pedigree structure. Risk factors were found in 69.5% of the remaining 679 patients, including 83 (12.2%) being heterozygotes for rare risk variants, in decreasing order of frequency, in TREM2, ABCA7, ATP8B4, SORL1, and ABCA1, including 5 heterozygotes for multiple rare risk variants, suggesting non-monogenic inheritance, even in some autosomal-dominant-like pedigrees., Conclusion: We suggest that genetic screening should be proposed to all EOAD patients and should no longer be prioritized based on pedigree structure., Competing Interests: Conflict of Interest The authors have no conflict of interest to declare., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
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- 2024
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241. Disfluency patterns in Alzheimer's disease and frontotemporal lobar degeneration.
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Pistono A, Pariente J, and Jucla M
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- Humans, Aged, Alzheimer Disease, Frontotemporal Lobar Degeneration, Frontotemporal Dementia
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Disfluencies may reflect various mechanisms: word-finding difficulties, planning strategies, inter-individual cognitive variability, etc. In the current paper, we examined disfluency production in patients with a behavioural variant of Frontotemporal lobar degeneration (bvFTLD), compared to patients with Alzheimer's disease (AD) and healthy older adults. We showed that bvFTLD participants have lower speech rate and produce more incomplete utterances. However, those measures were not correlated with naming and fluency tasks. On the contrary, AD participants did not differ from healthy controls on disfluency production, but discourse measures were correlated with the participants' lexical-semantic impairment. This provides evidence for different causes of disfluency in AD and FTLD, and a distinct role of each disfluency phenomenon.
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- 2024
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242. Robust thalamic nuclei segmentation from T1-weighted MRI using polynomial intensity transformation.
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Vidal JP, Danet L, Péran P, Pariente J, Cuadra MB, Zahr NM, Barbeau EJ, and Saranathan M
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Accurate segmentation of thalamic nuclei, crucial for understanding their role in healthy cognition and in pathologies, is challenging to achieve on standard T1-weighted (T1w) magnetic resonance imaging (MRI) due to poor image contrast. White-matter-nulled (WMn) MRI sequences improve intrathalamic contrast but are not part of clinical protocols or extant databases. In this study, we introduce histogram-based polynomial synthesis (HIPS), a fast preprocessing transform step that synthesizes WMn-like image contrast from standard T1w MRI using a polynomial approximation for intensity transformation. HIPS was incorporated into THalamus Optimized Multi-Atlas Segmentation (THOMAS) pipeline, a method developed and optimized for WMn MRI. HIPS-THOMAS was compared to a convolutional neural network (CNN)-based segmentation method and THOMAS modified for T1w images (T1w-THOMAS). The robustness and accuracy of the three methods were tested across different image contrasts (MPRAGE, SPGR, and MP2RAGE), scanner manufacturers (PHILIPS, GE, and Siemens), and field strengths (3T and 7T). HIPS-transformed images improved intra-thalamic contrast and thalamic boundaries, and HIPS-THOMAS yielded significantly higher mean Dice coefficients and reduced volume errors compared to both the CNN method and T1w-THOMAS. Finally, all three methods were compared using the frequently travelling human phantom MRI dataset for inter- and intra-scanner variability, with HIPS displaying the least inter-scanner variability and performing comparably with T1w-THOMAS for intra-scanner variability. In conclusion, our findings highlight the efficacy and robustness of HIPS in enhancing thalamic nuclei segmentation from standard T1w MRI.
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- 2024
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243. Effects of sociodemographic and player characteristics on baseline cognitive performance in 1000 rugby players: A retrospective 8-year follow-up study.
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Julien A, Tessier S, Tisserand C, Péran P, Planton M, Pariente J, and Brauge D
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- Male, Humans, Young Adult, Adult, Retrospective Studies, Follow-Up Studies, Rugby, Neuropsychological Tests, Cognition, Brain Concussion diagnosis, Brain Concussion psychology, Football, Athletic Injuries diagnosis
- Abstract
Objectives: To analyze the effects of sociodemographic and player characteristics on the Sport Concussion Assessment Tool and neuropsychological scores over 8 years in a large sample of rugby players., Design: An 8-year retrospective study of preseason clinical assessments of professional rugby players and players enrolled in training academies at professional clubs., Methods: The Sport Concussion Assessment Tool-3 or -5, Trail Making Test and Digit Symbol Substitution Test were administered prior to the start of the competition season for each player. Statistical analyses included: (i) descriptive analyses of sociodemographic, player and neuropsychological characteristics; (ii) multivariate models to identify factors influencing cognitive scores at the first visit; and (iii) linear mixed models to assess the evolution of the scores over the years., Results: One thousand players were included (mean age: 22.8, males: 92 %). Twenty-two percent of the athletes reported baseline symptoms. A higher level of education was associated with better cognitive scores at the first visit and over the years. Forwards had poorer processing speed performances compared to backs at the first visit and over repeated assessments. Finally, the number of examinations was associated with improved cognitive scores showing a practice effect on all the neuropsychological tests, except for the Standardized Assessment of Concussion 5th edition., Conclusions: Results from this retrospective study could help to improve the management of athletes and return-to-play decision-making in collision sports., Competing Interests: Declaration of interest statement The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)
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- 2023
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244. Physical activity, biomarkers of brain pathologies and dementia risk: Results from the Memento clinical cohort.
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Grasset L, Planche V, Bouteloup V, Azouani C, Dubois B, Blanc F, Paquet C, David R, Belin C, Jonveaux T, Julian A, Pariente J, Mangin JF, Chêne G, and Dufouil C
- Subjects
- Humans, Middle Aged, Aged, Amyloid beta-Peptides, Magnetic Resonance Imaging, Disease Progression, Biomarkers, Brain pathology, Atrophy pathology, tau Proteins, Dementia complications, Cognitive Dysfunction pathology, Alzheimer Disease pathology
- Abstract
Introduction: This study aims to examine whether physical activity moderates the association between biomarkers of brain pathologies and dementia risk., Methods: From the Memento cohort, we analyzed 1044 patients with mild cognitive impairment, aged 60 and older. Self-reported physical activity was assessed using the International Physical Activity Questionnaire. Biomarkers of brain pathologies comprised medial temporal lobe atrophy (MTA), white matter lesions, and plasma amyloid beta (Aβ)42/40 and phosphorylated tau181. Association between physical activity and risk of developing dementia over 5 years of follow-up, and interactions with biomarkers of brain pathologies were tested., Results: Physical activity moderated the association between MTA and plasma Aβ42/40 level and increased dementia risk. Compared to participants with low physical activity, associations of both MTA and plasma Aβ42/40 on dementia risk were attenuated in participants with high physical activity., Discussion: Although reverse causality cannot be excluded, this work suggests that physical activity may contribute to cognitive reserve., Highlights: Physical activity is an interesting modifiable target for dementia prevention. Physical activity may moderate the impact of brain pathology on dementia risk. Medial temporal lobe atrophy and plasma amyloid beta 42/40 ratio were associated with increased dementia risk especially in those with low level of physical activity., (© 2023 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.)
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- 2023
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245. Expressive Prosody in Patients With Focal Anterior Temporal Neurodegeneration.
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Geraudie A, Pressman PS, Pariente J, Millanski C, Palser ER, Ratnasiri BM, Battistella G, Mandelli ML, Miller ZA, Miller BL, Sturm V, Rankin KP, Gorno-Tempini ML, and Montembeault M
- Subjects
- Humans, Brain, Emotions, Empathy, Temporal Lobe diagnostic imaging, Cerebral Cortex, Magnetic Resonance Imaging, Frontotemporal Dementia diagnostic imaging, Aphasia, Primary Progressive psychology
- Abstract
Background and Objectives: Progressive focal anterior temporal lobe (ATL) neurodegeneration has been historically called semantic dementia. More recently, semantic variant primary progressive aphasia (svPPA) and semantic behavioral variant frontotemporal dementia (sbvFTD) have been linked with predominant left and right ATL neurodegeneration, respectively. Nonetheless, clinical tools for an accurate diagnosis of sbvFTD are still lacking. Expressive prosody refers to the modulation of pitch, loudness, tempo, and quality of voice used to convey emotional and linguistic information and has been linked to bilateral but right-predominant frontotemporal functioning. Changes in expressive prosody can be detected with semiautomated methods and could represent a useful diagnostic marker of socioemotional functioning in sbvFTD., Methods: Participants underwent a comprehensive neuropsychological and language evaluation and a 3T MRI at the University of California San Francisco. Each participant provided a verbal description of the picnic scene from the Western Aphasia Battery. The fundamental frequency (f0) range, an acoustic measure of pitch variability, was extracted for each participant. We compared the f0 range between groups and investigated associations with an informant-rated measure of empathy, a facial emotion labeling task, and gray matter (GM) volumes using voxel-based morphometry., Results: Twenty-eight patients with svPPA, 18 with sbvFTD, and 18 healthy controls (HCs) were included. f0 range was significantly different across groups: patients with sbvFTD showed reduced f0 range in comparison with both patients with svPPA (mean difference of -1.4 ± 2.4 semitones; 95% CI -2.4 to -0.4]; p < 0.005) and HCs (mean difference of -1.9 ± 3.0 semitones; 95% CI -3.0 to -0.7]; p < 0.001). A higher f0 range was correlated with a greater informant-rated empathy ( r = 0.355; p ≤ 0.05), but not facial emotion labeling. Finally, the lower f0 range was correlated with lower GM volume in the right superior temporal gyrus, encompassing anterior and posterior portions ( p < 0.05 FWE cluster corrected)., Discussion: Expressive prosody may be a useful clinical marker of sbvFTD. Reduced empathy is a core symptom in sbvFTD; the present results extend this to prosody, a core component of social interaction, at the intersection of speech and emotion. They also inform the long-standing debate on the lateralization of expressive prosody in the brain, highlighting the critical role of the right superior temporal lobe., (© 2023 American Academy of Neurology.)
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- 2023
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246. Clinical heterogeneity of neuro-inflammatory PET profiles in early Alzheimer's disease.
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Gouilly D, Salabert AS, Bertrand E, Goubeaud M, Catala H, Germain J, Ainaoui N, Rafiq M, Benaiteau M, Carlier J, Nogueira L, Planton M, Hitzel A, Méligne D, Sarton B, Silva S, Lemesle B, Payoux P, Thalamas C, Péran P, and Pariente J
- Abstract
The relationship between neuroinflammation and cognition remains uncertain in early Alzheimer's disease (AD). We performed a cross-sectional study to assess how neuroinflammation is related to cognition using TSPO PET imaging and a multi-domain neuropsychological assessment. A standard uptake value ratio (SUVR) analysis was performed to measure [
18 F]-DPA-714 binding using the cerebellar cortex or the whole brain as a (pseudo)reference region. Among 29 patients with early AD, the pattern of neuroinflammation was heterogeneous and exhibited no correlation with cognition at voxel-wise, regional or whole-brain level. The distribution of the SUVR values was independent of sex, APOE phenotype, early and late onset of symptoms and the presence of cerebral amyloid angiopathy. However, we were able to demonstrate a complex dissociation as some patients with similar PET pattern had opposed neuropsychological profiles while other patients with opposite PET profiles had similar neuropsychological presentation. Further studies are needed to explore how this heterogeneity impacts disease progression., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Gouilly, Salabert, Bertrand, Goubeaud, Catala, Germain, Ainaoui, Rafiq, Benaiteau, Carlier, Nogueira, Planton, Hitzel, Méligne, Sarton, Silva, Lemesle, Payoux, Thalamas, Péran and Pariente.)- Published
- 2023
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247. Longitudinal head-to-head comparison of 11 C-PiB and 18 F-florbetapir PET in a Phase 2/3 clinical trial of anti-amyloid-β monoclonal antibodies in dominantly inherited Alzheimer's disease.
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Chen CD, McCullough A, Gordon B, Joseph-Mathurin N, Flores S, McKay NS, Hobbs DA, Hornbeck R, Fagan AM, Cruchaga C, Goate AM, Perrin RJ, Wang G, Li Y, Shi X, Xiong C, Pontecorvo MJ, Klein G, Su Y, Klunk WE, Jack C, Koeppe R, Snider BJ, Berman SB, Roberson ED, Brosch J, Surti G, Jiménez-Velázquez IZ, Galasko D, Honig LS, Brooks WS, Clarnette R, Wallon D, Dubois B, Pariente J, Pasquier F, Sanchez-Valle R, Shcherbinin S, Higgins I, Tunali I, Masters CL, van Dyck CH, Masellis M, Hsiung R, Gauthier S, Salloway S, Clifford DB, Mills S, Supnet-Bell C, McDade E, Bateman RJ, and Benzinger TLS
- Subjects
- Humans, Amyloid beta-Peptides metabolism, Positron-Emission Tomography methods, Aniline Compounds, Ethylene Glycols, Brain metabolism, Alzheimer Disease diagnostic imaging, Alzheimer Disease drug therapy
- Abstract
Purpose: Pittsburgh Compound-B (
11 C-PiB) and18 F-florbetapir are amyloid-β (Aβ) positron emission tomography (PET) radiotracers that have been used as endpoints in Alzheimer's disease (AD) clinical trials to evaluate the efficacy of anti-Aβ monoclonal antibodies. However, comparing drug effects between and within trials may become complicated if different Aβ radiotracers were used. To study the consequences of using different Aβ radiotracers to measure Aβ clearance, we performed a head-to-head comparison of11 C-PiB and18 F-florbetapir in a Phase 2/3 clinical trial of anti-Aβ monoclonal antibodies., Methods: Sixty-six mutation-positive participants enrolled in the gantenerumab and placebo arms of the first Dominantly Inherited Alzheimer Network Trials Unit clinical trial (DIAN-TU-001) underwent both11 C-PiB and18 F-florbetapir PET imaging at baseline and during at least one follow-up visit. For each PET scan, regional standardized uptake value ratios (SUVRs), regional Centiloids, a global cortical SUVR, and a global cortical Centiloid value were calculated. Longitudinal changes in SUVRs and Centiloids were estimated using linear mixed models. Differences in longitudinal change between PET radiotracers and between drug arms were estimated using paired and Welch two sample t-tests, respectively. Simulated clinical trials were conducted to evaluate the consequences of some research sites using11 C-PiB while other sites use18 F-florbetapir for Aβ PET imaging., Results: In the placebo arm, the absolute rate of longitudinal change measured by global cortical11 C-PiB SUVRs did not differ from that of global cortical18 F-florbetapir SUVRs. In the gantenerumab arm, global cortical11 C-PiB SUVRs decreased more rapidly than global cortical18 F-florbetapir SUVRs. Drug effects were statistically significant across both Aβ radiotracers. In contrast, the rates of longitudinal change measured in global cortical Centiloids did not differ between Aβ radiotracers in either the placebo or gantenerumab arms, and drug effects remained statistically significant. Regional analyses largely recapitulated these global cortical analyses. Across simulated clinical trials, type I error was higher in trials where both Aβ radiotracers were used versus trials where only one Aβ radiotracer was used. Power was lower in trials where18 F-florbetapir was primarily used versus trials where11 C-PiB was primarily used., Conclusion: Gantenerumab treatment induces longitudinal changes in Aβ PET, and the absolute rates of these longitudinal changes differ significantly between Aβ radiotracers. These differences were not seen in the placebo arm, suggesting that Aβ-clearing treatments may pose unique challenges when attempting to compare longitudinal results across different Aβ radiotracers. Our results suggest converting Aβ PET SUVR measurements to Centiloids (both globally and regionally) can harmonize these differences without losing sensitivity to drug effects. Nonetheless, until consensus is achieved on how to harmonize drug effects across radiotracers, and since using multiple radiotracers in the same trial may increase type I error, multisite studies should consider potential variability due to different radiotracers when interpreting Aβ PET biomarker data and, if feasible, use a single radiotracer for the best results., Trial Registration: ClinicalTrials.gov NCT01760005. Registered 31 December 2012. Retrospectively registered., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)- Published
- 2023
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248. [Neurological forms of long COVID in adults: Critical approach].
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Chollet F, Planton M, Sailler L, De Almeida S, Alvarez M, and Pariente J
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Now recognized by health authorities, long COVID is identified as a frequent condition complicating the evolution of SARS-CoV-2 infection. Its polymorphic and sometimes disconcerting clinical expression raises questions about its mechanism. Patterns of clinical expression suggest extensive involvement of the nervous system through an almost ubiquitous cognitive complaint. This article reviews the neurological symptoms and forms of these patients, and the neuropsychological explorations aimed at objectifying a cognitive deficit. The studies published until now confronted with the clinical mode of expression, did not make it possible to define a deficit neuropsychological profile at the level of the groups, and evoked more a functional impairment than a lesion. However, each series mentions a small number of patients in whom a cognitive deficit is objectified. The uncertainties about the causes of the prolonged forms of COVID, the heterogeneity of the published studies, and the virtual absence of temporal evolution data should make one cautious about the interpretation of these data but should in no way delay or prevent taking into account care of these patients., (© 2023 l'Académie nationale de médecine. Published by Elsevier Masson SAS. All rights reserved.)
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- 2023
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249. Impact of a pediatric posterior fossa tumor and its treatments on motor procedural learning.
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Baudou E, Danna J, Tallet J, Pollidoro L, Tensaouti F, Bertozzi AI, Pariente J, Courbieres N, Dufour C, Grill J, Chaix Y, and Laprie A
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- Child, Humans, Cerebellum pathology, Corpus Striatum, Motor Skills, Neostriatum, Infratentorial Neoplasms radiotherapy, Infratentorial Neoplasms pathology, Learning
- Abstract
Introduction: Posterior fossa tumor (PFT) survivors have difficulty learning new skills. Procedural memory is a skill learning system that allows, through training, the automatization of procedures and progressive improvement of performance. It underlies most of the motor procedures in everyday life that we perform automatically, such as riding a bike or writing. Motor procedural memory is divided into two components: motor sequence learning involving mainly cortico-striatal networks, and motor adaptation involving mainly cortico-cerebellar networks. The aim of this work was to explore the impact of a tumor and its treatment during childhood on procedural learning hypothesizing that sequence learning would be impaired in PFT survivors who have been treated with radiotherapy, whereas motor adaptation would be impaired in all PFT survivors., Method: 22 irradiated survivors of PFT, 17 non-irradiated survivors and 21 healthy controls from the IMPALA study (NCT04324450) performed a motor sequence learning task and a motor adaptation task. Doses received by striatal and cerebellar structures were reported from the initial dosimetry plans., Results: Sequence learning was preserved in both tumor groups, but at the individual level 7/22 irradiated, and 4/17 non-irradiated participants failed to learn the motor sequence. Motor adaptation was impaired in both tumor groups, predominantly in the irradiated group., Conclusion: This study sheds new light on the long-term impact of PFT treatments in childhood on a rarely-studied part of memory, which is perceptual-motor procedural learning. Our results suggest that the cerebellum and striatum could be considered as organs at risk with regard to procedural learning., Competing Interests: Declaration of competing interest The authors have stated that they had no interests which might be perceived as posing a conflict or bias., (© 2023 Published by Elsevier Ltd on behalf of European Paediatric Neurology Society.)
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- 2023
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250. Cerebrospinal fluid YKL-40 level evolution is associated with autoimmune encephalitis remission.
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Dorcet G, Benaiteau M, Pariente J, Ory-Magne F, Cheuret E, Rafiq M, Brooks W, Puissant-Lubrano B, Fortenfant F, Renaudineau Y, and Bost C
- Abstract
Objective: Because of its heterogeneity in clinical presentation and course, predicting autoimmune encephalitis (AIE) evolution remains challenging. Hence, our aim was to explore the correlation of several biomarkers with the clinical course of disease., Methods: Thirty-seven cases of AIE were selected retrospectively and divided into active ( N = 9), improved ( N = 12) and remission ( N = 16) AIE according to their disease evolution. Nine proteins were tested in both serum and cerebrospinal fluid (CSF) at diagnosis (T0) and during the follow-up (T1), in particular activated MMP-9 (MMP-9A) and YKL-40 (or chitinase 3-like 1)., Results: From diagnosis to revaluation, AIE remission was associated with decreased YKL-40 and MMP-9A levels in the CSF, and with decreased NfL and NfH levels in the serum. The changes in YKL-40 concentrations in the CSF were associated with (1) still active AIE when increasing >10% ( P- value = 0.0093); (2) partial improvement or remission when the changes were between +9% and -20% ( P- value = 0.0173); and remission with a reduction > -20% (P- value = 0.0072; overall difference between the three groups: P- value = 0.0088). At T1, the CSF YKL-40 levels were significantly decreased between active and improved as well as improved and remission AIE groups but with no calculable threshold because of patient heterogeneity., Conclusion: The concentration of YKL-40, a cytokine-like proinflammatory protein produced by glial cells, is correlated in the CSF with the clinical course of AIE. Its introduction as a biomarker may assist in following disease activity and in evaluating therapeutic response., Competing Interests: The authors declare no conflict of interest., (© 2023 The Authors. Clinical & Translational Immunology published by John Wiley & Sons Australia, Ltd on behalf of Australian and New Zealand Society for Immunology, Inc.)
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- 2023
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