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1. Characteristics and progression of patients with frontotemporal dementia in a regional memory clinic network

Author

Mélanie Leroy, Maxime Bertoux, Emilie Skrobala, Elisa Mode, Catherine Adnet-Bonte, Isabelle Le Ber, Stéphanie Bombois, Pascaline Cassagnaud, Yaohua Chen, Vincent Deramecourt, Florence Lebert, Marie Anne Mackowiak, Adeline Rollin Sillaire, Marielle Wathelet, Florence Pasquier, Thibaud Lebouvier, and the Méotis network

Subjects
Frontotemporal dementia, Epidemiology, Progression, Dementia, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Due to heterogeneous clinical presentation, difficult differential diagnosis with Alzheimer’s disease (AD) and psychiatric disorders, and evolving clinical criteria, the epidemiology and natural history of frontotemporal lobar degeneration (FTD) remain elusive. In order to better characterize FTD patients, we relied on the database of a regional memory clinic network with standardized diagnostic procedures and chose AD patients as a comparator. Methods Patients that were first referred to our network between January 2010 and December 2016 and whose last clinical diagnosis was degenerative or vascular dementia were included. Comparisons were conducted between FTD and AD as well as between the different FTD syndromes, divided into language variants (lvFTD), behavioral variant (bvFTD), and FTD with primarily motor symptoms (mFTD). Cognitive progression was estimated with the yearly decline in Mini Mental State Examination (MMSE). Results Among the patients that were referred to our network in the 6-year time span, 690 were ultimately diagnosed with FTD and 18,831 with AD. Patients with FTD syndromes represented 2.6% of all-cause dementias. The age-standardized incidence was 2.90 per 100,000 person-year and incidence peaked between 75 and 79 years. Compared to AD, patients with FTD syndromes had a longer referral delay and delay to diagnosis. Patients with FTD syndromes had a higher MMSE score than AD at first referral while their progression was similar. mFTD patients had the shortest survival while survival in bvFTD, lvFTD, and AD did not significantly differ. FTD patients, especially those with the behavioral variant, received more antidepressants, anxiolytics, and antipsychotics than AD patients. Conclusions FTD syndromes differ with AD in characteristics at baseline, progression rate, and treatment. Despite a broad use of the new diagnostic criteria in an organized memory clinic network, FTD syndromes are longer to diagnose and account for a low proportion of dementia cases, suggesting persistent underdiagnosis. Congruent with recent publications, the late peak of incidence warns against considering FTD as being exclusively a young-onset dementia.

Published
2021
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2. The topography of cortical microbleeds in frontotemporal lobar degeneration: a post-mortem 7.0-tesla magnetic resonance study

Author

Jacques De Reuck, Florent Auger, Nicolas Durieux, Vincent Deramecourt, Claude-Alain Maurage, Florence Lebert, Didier Leys, Charlotte Cordonnier, Florence Pasquier, and Regis Bordet

Subjects
7.0-tesla magnetic resonance imaging, topography of post-mortem cortical microbleeds, frontotemporal lobar degeneration, neurodegenerative diseases, Medicine
Abstract

Introduction : Cerebrovascular lesions are rare in frontotemporal lobar degeneration (FTLD), in contrast to other neurodegenerative diseases. Cortical microbleeds (CoMBs) are frequent in Alzheimer’s disease, in particular in cases associated with cerebral amyloid angiopathy. The present study investigates the gyral topographic distribution of CoMBs in post-mortem FTLD brains with 7.0-tesla magnetic resonance imaging. Material and methods : The distribution of CoMBs in 11 post-mortem FTLD brains and in 12 control brains was compared on T2*-GRE MRI of six coronal sections of a cerebral hemisphere. The mean values of CoMBs were determined in twenty-two different gyri. The findings were correlated to those separately observed on neuropathological examination. Results : As a whole there was a trend of more CoMBs in the prefrontal section of FTLD as well as of the control brains. CoMBs were significantly increased in the superior frontal gyrus and the insular cortex (p ≤ 0.001) and also in the inferior frontal gyrus and the superior temporal gyrus (p ≤ 0.01). Conclusions : CoMBs in FTLD are only increased in the regions mainly affected by the neurodegenerative lesions. They probably do not reflect additional cerebrovascular disease.

Published
2016
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3. DAPHNE: A New Tool for the Assessment of the Behavioral Variant of Frontotemporal Dementia

Author

Claire Boutoleau-Bretonnière, Christelle Evrard, Jean Benoît Hardouin, Laëtitia Rocher, Tiphaine Charriau, Frédérique Etcharry-Bouyx, Sophie Auriacombe, Aurélie Richard-Mornas, Florence Lebert, Florence Pasquier, Anne Sauvaget, Samuel Bulteau, Martine Vercelletto, Pascal Derkinderen, Cédric Bretonnière, and Catherine Thomas-Antérion

Subjects
Frontotemporal dementia, Behavioral disorders, Alzheimer’s disease, Bipolar disorder, Progressive supranuclear palsy, Scale, Neurology. Diseases of the nervous system, RC346-429, Geriatrics, RC952-954.6
Abstract

Background: The diagnosis of behavioral variant of frontotemporal dementia (bvFTD) relies primarily on clinical features and remains challenging. The specificity of the recently revised criteria can be disappointing, justifying development of new clinical tools. Objective: We produced a behavioral inventory named DAPHNE. This scale (adapted from Rascovsky's criteria) explores six domains: disinhibition, apathy, perseverations, hyperorality, personal neglect and loss of empathy. It is composed of ten items (five answer categories). The aim was (1) to assess the validity and reliability of DAPHNE and (2) to evaluate its contribution in differentiating patients. Methods: Two scores were computed: DAPHNE-6 (screening) from the six domains and DAPHNE-40 (diagnosis) from the ten items. Reliability and reproducibility were assessed. External validity was studied with the Frontal Behavioral Inventory (FBI) and the Frontotemporal Behavioral Scale (FBS). Finally, the diagnostic performance of DAPHNE was compared to revised criteria, FBI and FBS. Results: DAPHNE was administered to the caregivers of 89 patients, 36 with bvFTD, 22 with Alzheimer's disease, 15 with progressive supranuclear palsy and 16 with bipolar disorder. Reliability and reproducibility were excellent, as was external validity. DAPHNE-6 allowed bvFTD diagnosis (score ≥4) with a sensitivity of 92%, while DAPHNE-40 (score ≥15) had a specificity of 92%. Conclusion: We demonstrate excellent psychometric features for DAPHNE. This quick tool could help for both diagnosing and screening bvFTD.

Published
2015
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4. Reducing Employment Insecurity

Author

Florence Lebert and Erika Antal

Subjects
History of scholarship and learning. The humanities, AZ20-999, Social Sciences
Abstract

The perception of job insecurity is known to be a stressful condition for employees. Less is known about employment insecurity and the ways employees and their families deal with it. This study investigates whether participation in further training is a strategy that employees adopt to reduce perceived employment insecurity. As participation in further training is often costly and time-consuming, we assume that the family context is of importance for the decision to take part in further training. To take account of possible self-selection, we apply a propensity score matching procedure on longitudinal data from the Swiss Household Panel (2004-2013). Three main findings can be emphasized: first, participation in further training is not a strategy adopted particularly by employees who perceive high employment insecurity as they are less likely to train than their secure counterparts. Second, even though further training is not a strategy that is actively adopted, employees who train subsequently report lower levels of perceived employment insecurity. Third, the family context indeed influences the likelihood to train: partnered employees are more likely to train and preschool-aged children act as a constraint on women’s but enhance men’s participation in further training. Yet, in the context of high perceived employment insecurity, children generally reduce their parents’ likelihood to train as the parents may turn to other strategies that reduce perceived employment insecurity.

Published
2016
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5. Voluntary Turnover: A Means of Reducing Perceived Job Insecurity? A Propensity Score Matching Procedure Applied on Swiss Data

Author

Florence Lebert

Subjects
job insecurity, coping, voluntary turnover, family, Switzerland, Swiss Household Panel, propensity score matching, Social Sciences
Abstract

The investigation of job insecurity has been a growing field of research. However, little is known about the strategies employees adopt to reduce job insecurity. Former research has shown that employees who perceive high job insecurity tend to engage in voluntary turnover. Yet, we do not know whether such a strategy is successful in reducing perceived job insecurity. Based on the Swiss Household Panel (SHP), a general population survey in Switzerland, a propensity score matching procedure is applied to investigate whether voluntary turnover successfully reduces feelings of job insecurity for employees who previously perceived an above-average level of job insecurity. Assuming that individual and family conditions are important factors explaining the success of this strategy it is distinguished between men and women with high, equally shared, or low financial responsibilities and of different age and educational groups. The results show that voluntary turnover indeed reduces perceived job insecurity. Whereas the individual factors do not moderate this relationship, the level of financial responsibilities does: employees who equally share financial responsibilities with their partners are most successful in reducing perceived job insecurity through voluntary turnover. The use of a propensity score matching procedure has proven fruitful as the bias caused by differing pre-turnover characteristics can be reduced considerably.

Published
2016
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6. The gendered consequences of the COVID-19 lockdown on unpaid work in Swiss dual earner couples with children

Author

Stephanie Steinmetz, Leen Vandecasteele, Florence Lebert, Marieke Voorpostel, Oliver Lipps, and Institutions, Inequalities, and Life courses (IIL, AISSR, FMG)

Subjects
Gender Studies, Organizational Behavior and Human Resource Management, 300 Social sciences, sociology & anthropology
Abstract

This article assesses the gendered impact of COVID-19 measures on changes in time that Swiss dual earner couples spent on unpaid work during the pandemic, focusing on families with children. Overcoming some of the methodological shortcomings of previous studies, high-quality representative panel data allow us to examine the change in time invested in housework and childcare before and during the pandemic, and test theoretical assumptions as to the mechanisms underlying the observed patterns. Gender inequalities are explained by the couple's work division prior to, and at the onset of, the pandemic and interpreted in the light of key theoretical approaches (economics of the family, bargaining and time availability, doing gender). Our results imply that in particular changes in the time availability of the partner are relevant for changes in time spent on housework, while in case of care work, the own time availability matters more. Moreover, we also found that the respondents' economic bargaining power within the couple matters both for housework and care work. Finally, the implemented COVID-19 measures neither led to an increase in patriarchal power structures nor did they foster an increase in equality for unpaid work among women and men. Instead, the results show that changes in time availability due to short-time, remote or overtime working schemes determined changes in time spent on unpaid care to a larger extent than gender alone.

Published
2022
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7. The Swiss Household Panel (SHP)

Author

Robin Tillmann, Nora Dasoki, Marieke Voorpostel, Florence Lebert, Gian-Andrea Monsch, Valérie-Anne Ryser, Ursina Kuhn, Erika Antal, and Hannah S. Klaas

Subjects
Economics and Econometrics, Longitudinal data, Life course approach, Psychology, General Business, Management and Accounting, Social Sciences (miscellaneous), Demography
Abstract

Collecting data on households and individuals since 1999, the Swiss Household Panel (SHP) is an ongoing, unique, large-scale, nationally representative, longitudinal study in Switzerland (N = 9828 households and N = 15,882 persons interviewed in 2020). The SHP aims to provide both continuity and innovation in measurement and data collection. Examples of innovation are the combination of retrospective and prospective longitudinal data, the combination of survey modes notably in refreshment samples and additional studies oversampling specific population groups. This article provides an overview of the SHP – focusing on the survey’s key design features, content, data collection and adjustments, possibilities for cross-national comparisons, data use and accomplishments.

Published
2021

8. Characteristics of Bipolar Patients with Cognitive Impairment of Suspected Neurodegenerative Origin: A Multicenter Cohort

Author

Emilie Olié, Emmanuel Cognat, Djamila Bennabi, Esteban Munoz Musat, Frédéric Blanc, Florence Lebert, Eloi Magnin, Audrey Gabelle, Claire Paquet, Mélanie Leroy, Emeline Marlinge, Magnin, Eloi, Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Lille Neurosciences & Cognition - U 1172 (LilNCog), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), 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), Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre Mémoire de Ressources et de Recherche [Lille-Bailleul] (CMRR), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Hôpital Roger Salengro [Lille], Institut des Neurosciences de Montpellier (INM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Laboratoire de Neurosciences Intégratives et Cliniques - UFC (UR 481) (NEURO), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre d'Investigation Clinique de Besançon (Inserm CIC 1431), Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), Centre Mémoire Ressources et Recherche [Strasbourg] (CMRR Strasbourg), CHU Strasbourg, Laboratoire des sciences de l'ingénieur, de l'informatique et de l'imagerie (ICube), École Nationale du Génie de l'Eau et de l'Environnement de Strasbourg (ENGEES)-Université de Strasbourg (UNISTRA)-Institut National des Sciences Appliquées - Strasbourg (INSA Strasbourg), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de Recherche en Informatique et en Automatique (Inria)-Les Hôpitaux Universitaires de Strasbourg (HUS)-Centre National de la Recherche Scientifique (CNRS)-Matériaux et Nanosciences Grand-Est (MNGE), Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Réseau nanophotonique et optique, Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg (UNISTRA), Optimisation thérapeutique en Neuropsychopharmacologie (OPTeN (UMR_S_1144 / U1144)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), and Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS BFC)-Université de Franche-Comté (UFC)

Subjects
cognition, medicine.medical_specialty, [SDV]Life Sciences [q-bio], Medicine (miscellaneous), Parkinsonism, Article, Internal medicine, medicine, Dementia, Bipolar disorder, bipolar disorder, business.industry, neurodegenerescence, Neuropsychology, biomarkers, Cognition, medicine.disease, [SDV] Life Sciences [q-bio], Biomarker (medicine), Medicine, business, Neurocognitive, Alzheimer’s disease, Executive dysfunction, dementia
Abstract

Bipolar disorder is associated with an increased risk of dementia with aging. Little is known regarding this association, limiting appropriate diagnosis and management. We aimed to describe the characteristics of bipolar patients with late cognitive impairment for whom the hypothesis of an underlying neurodegenerative disease had been raised. We performed a retrospective multicenter study, recruiting bipolar patients over 50 years old from five French tertiary memory centers who had undergone cerebrospinal fluid (CSF) biomarker assessment for Alzheimer’s disease (AD). Clinical, neuropsychological, and paraclinical characteristics were analyzed and 78 patients were included. The mean age at the onset of cognitive impairment was 62.4 years (±9.2). The mean MMSE score was 22.8 (±4.5), the mean FAB was 11.7 (±3.9), and the mean FCRST was 15.8 (±7.4)/36.8 (±9.7) (free/total recall). A total of 48.6% of the patients displayed cognitive fluctuations, and 38.2% showed cognitive improvement during follow-ups, and 56.3% of the patients showed Parkinsonism, of which 12.7% had never received antipsychotics. Among patients who underwent DAT-scans, 35.3% displayed dopaminergic denervation, 10.3% of patients had CSF AD biological signature (“A+ T+” profile), while 56.4% had other abnormal CSF profiles. Thus, clinical presentation was dominated by executive dysfunction, episodic memory impairment, fluctuating cognition, and a high frequency of Parkinsonism. Specifically, high frequency of delusional episodes suggests limited tolerance of psychotropic drugs. Most patients had abnormal CSF biomarker profiles, but only a minority displayed AD’s specific biomarker signature. Therefore, while our results unveil shared common neurocognitive features in bipolar patients with cognitive impairment of suspected neurodegenerative origin they suggest a participation of various underlying pathologies rather than a common degenerative mechanism in the pathophysiology of this condition.

Published
2021
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9. Gene Expression Imputation Across Multiple Tissue Types Provides Insight Into the Genetic Architecture of Frontotemporal Dementia and Its Clinical Subtypes

Author

Lianne M. Reus, Bogdan Pasaniuc, Danielle Posthuma, Toni Boltz, Yolande A.L. Pijnenburg, Roel A. Ophoff, Raffaele Ferrari, Dena G. Hernandez, Michael A. Nalls, Jonathan D. Rohrer, Adaikalavan Ramasamy, John B.J. Kwok, Carol Dobson-Stone, William S. Brooks, Peter R. Schofield, Glenda M. Halliday, John R. Hodges, Olivier Piguet, Lauren Bartley, Elizabeth Thompson, Isabel Hernández, Agustín Ruiz, Mercè Boada, Barbara Borroni, Alessandro Padovani, Carlos Cruchaga, Nigel J. Cairns, Luisa Benussi, Giuliano Binetti, Roberta Ghidoni, Gianluigi Forloni, Daniela Galimberti, Chiara Fenoglio, Maria Serpente, Elio Scarpini, Jordi Clarimón, Alberto Lleó, Rafael Blesa, Maria Landqvist Waldö, Karin Nilsson, Christer Nilsson, Ian R.A. Mackenzie, Ging-Yuek R. Hsiung, David M.A. Mann, Jordan Grafman, Christopher M. Morris, Johannes Attems, Timothy D. Griffiths, Ian G. McKeith, Alan J. Thomas, Pietro Pietrini, Edward D. Huey, Eric M. Wassermann, Atik Baborie, Evelyn Jaros, Michael C. Tierney, Pau Pastor, Cristina Razquin, Sara Ortega-Cubero, Elena Alonso, Robert Perneczky, Janine Diehl-Schmid, Panagiotis Alexopoulos, Alexander Kurz, Innocenzo Rainero, Elisa Rubino, Lorenzo Pinessi, Ekaterina Rogaeva, Peter St. George-Hyslop, Giacomina Rossi, Fabrizio Tagliavini, Giorgio Giaccone, James B. Rowe, Johannes C.M. Schlachetzki, James Uphill, John Collinge, Simon Mead, Adrian Danek, Vivianna M. Van Deerlin, Murray Grossman, John Q. Trojanowski, Julie van der Zee, Christine Van Broeckhoven, Stefano F. Cappa, Isabelle Le Ber, Didier Hannequin, Véronique Golfier, Martine Vercelletto, Alexis Brice, Benedetta Nacmias, Sandro Sorbi, Silvia Bagnoli, Irene Piaceri, Jørgen E. Nielsen, Lena E. Hjermind, Matthias Riemenschneider, Manuel Mayhaus, Bernd Ibach, Gilles Gasparoni, Sabrina Pichler, Wei Gu, Martin N. Rossor, Nick C. Fox, Jason D. Warren, Maria Grazia Spillantini, Huw R. Morris, Patrizia Rizzu, Peter Heutink, Julie S. Snowden, Sara Rollinson, Anna Richardson, Alexander Gerhard, Amalia C. Bruni, Raffaele Maletta, Francesca Frangipane, Chiara Cupidi, Livia Bernardi, Maria Anfossi, Maura Gallo, Maria Elena Conidi, Nicoletta Smirne, Rosa Rademakers, Matt Baker, Dennis W. Dickson, Neill R. Graff-Radford, Ronald C. Petersen, David Knopman, Keith A. Josephs, Bradley F. Boeve, Joseph E. Parisi, William W. Seeley, Bruce L. Miller, Anna M. Karydas, Howard Rosen, John C. van Swieten, Elise G.P. Dopper, Harro Seelaar, Philip Scheltens, Giancarlo Logroscino, Rosa Capozzo, Valeria Novelli, Annibale A. Puca, Massimo Franceschi, Alfredo Postiglione, Graziella Milan, Paolo Sorrentino, Mark Kristiansen, Huei-Hsin Chiang, Caroline Graff, Florence Pasquier, Adeline Rollin, Vincent Deramecourt, Florence Lebert, Dimitrios Kapogiannis, Luigi Ferrucci, Stuart Pickering-Brown, Andrew B. Singleton, John Hardy, Parastoo Momeni, Complex Trait Genetics, Amsterdam Neuroscience - Complex Trait Genetics, Child and Adolescent Psychiatry / Psychology, Erasmus MC other, Neurology, Psychiatry, Human genetics, Amsterdam Neuroscience - Compulsivity, Impulsivity & Attention, Amsterdam Reproduction & Development (AR&D), and Amsterdam Neuroscience - Neurodegeneration

Subjects
0301 basic medicine, Candidate gene, 17q21.31 inversion region, Dorsolateral prefrontal cortex, Expression quantitative trait loci (eQTL), Frontotemporal dementia, SEC22B, Transcriptome-wide association study, Semantic dementia, Gene Expression, Locus (genetics), Biology, 03 medical and health sciences, 0302 clinical medicine, Progressive nonfluent aphasia, mental disorders, medicine, Humans, Gene, Biological Psychiatry, Genetics, nutritional and metabolic diseases, medicine.disease, Genetic architecture, nervous system diseases, 030104 developmental biology, medicine.anatomical_structure, Frontotemporal Dementia, 030217 neurology & neurosurgery
Abstract

Background: The etiology of frontotemporal dementia (FTD) is poorly understood. To identify genes with predicted expression levels associated with FTD, we integrated summary statistics with external reference gene expression data using a transcriptome-wide association study approach. Methods: FUSION software was used to leverage FTD summary statistics (all FTD: n = 2154 cases, n = 4308 controls; behavioral variant FTD: n = 1337 cases, n = 2754 controls; semantic dementia: n = 308 cases, n = 616 controls; progressive nonfluent aphasia: n = 269 cases, n = 538 controls; FTD with motor neuron disease: n = 200 cases, n = 400 controls) from the International FTD-Genomics Consortium with 53 expression quantitative loci tissue type panels (n = 12,205; 5 consortia). Significance was assessed using a 5% false discovery rate threshold. Results: We identified 73 significant gene–tissue associations for FTD, representing 44 unique genes in 34 tissue types. Most significant findings were derived from dorsolateral prefrontal cortex splicing data (n = 19 genes, 26%). The 17q21.31 inversion locus contained 23 significant associations, representing 6 unique genes. Other top hits included SEC22B (a gene involved in vesicle trafficking), TRGV5, and ZNF302. A single gene finding (RAB38) was observed for behavioral variant FTD. For other clinical subtypes, no significant associations were observed. Conclusions: We identified novel candidate genes (e.g., SEC22B) and previously reported risk regions (e.g., 17q21.31) for FTD. Most significant associations were observed in dorsolateral prefrontal cortex splicing data despite the modest sample size of this reference panel. This suggests that our findings are specific to FTD and are likely to be biologically relevant highlights of genes at different FTD risk loci that are contributing to the disease pathology.

Published
2021
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10. Alzheimer's disease phenotypes misdiagnosed with frontotemporal lobar degeneration: A retrospective neuropathologic study

Author

Claude Alain Maurage, Melanie Leroy, Florence Pasquier, Simon Lecerf, Vincent Deramecourt, Florence Lebert, and Thibaud Lebouvier

Subjects
Pathology, medicine.medical_specialty, Epidemiology, business.industry, Health Policy, Neuropathology, Frontotemporal lobar degeneration, medicine.disease, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, medicine, Neurology (clinical), Geriatrics and Gerontology, Clinical phenotype, business
Published
2020
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11. Who is most affected by the Corona crisis? An analysis of changes in stress and well-being in Switzerland

Author

Ursina Kuhn, Jan-Erik Refle, Hannah S. Klaas, Oliver Lipps, Florence Lebert, Valérie-Anne Ryser, Gian-Andrea Monsch, Erika Antal, Robin Tillmann, Nora Dasoki, and Marieke Voorpostel

Subjects
Coronavirus disease 2019 (COVID-19), 05 social sciences, Geography, Planning and Development, Vulnerability, 050109 social psychology, 0506 political science, Geography, Stress (linguistics), Well-being, 050602 political science & public administration, medicine, 0501 psychology and cognitive sciences, Demographic economics, Social isolation, medicine.symptom, Demography, Panel data
Abstract

This study analyses the consequences of the Covid-19 crisis on stress and well-being in Switzerland. In particular, we assess whether vulnerable groups in terms of social isolation, increased workl...

Published
2020

12. What the COVID-19 pandemic entails for the management of patients with behavioral and psychological symptoms of dementia: experience in France

Author

Alexis Lepetit, Saidlitz Pascal, Lisette Volpe-Gillot, Florence Lebert, Olivier Drunat, Hermine Lenoir, Pierre Koskas, Samuel Kohler, Maria Soto-Martin, Jean Roche, Mouna Romdhani, Vania Leclercq, and Vernaudon Julien

Subjects
medicine.medical_specialty, Coronavirus disease 2019 (COVID-19), Disease Outbreaks, Pandemic, medicine, Humans, Dementia, Psychiatry, Pandemics, Aged, Aged, 80 and over, Problem Behavior, SARS-CoV-2, business.industry, COVID-19, medicine.disease, Patient Care Management, Psychiatry and Mental health, Clinical Psychology, Practice Guidelines as Topic, Commentary, France, Geriatrics and Gerontology, business, Gerontology
Published
2020
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13. Neurobiol Aging

Author

Pascaline Cassagnaud, David Wallon, Vincent Deramecourt, Florence Pasquier, Didier Hannequin, NeuroCEB Brain Bank, Thibaud Lebouvier, Sophie Auriacombe, Bruno Dubois, Mathieu Ceccaldi, Claude-Alain Maurage, Isabelle Le Ber, Marie Sarazin, Florence Lebert, Maxime Bertoux, Bordeaux population health (BPH), and 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)

Subjects
Male, 0301 basic medicine, Aging, Pathology, medicine.medical_specialty, Amnesia, Autopsy, Disease, Neuropsychological Tests, SEPIA, 03 medical and health sciences, Cognition, 0302 clinical medicine, Alzheimer Disease, Memory, Predictive Value of Tests, medicine, Humans, Dementia, Cognitive decline, Pathological, Aged, Cued speech, Verbal Behavior, business.industry, General Neuroscience, Middle Aged, medicine.disease, 030104 developmental biology, Female, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Neurology (clinical), Cues, Geriatrics and Gerontology, Verbal memory, medicine.symptom, business, 030217 neurology & neurosurgery, Developmental Biology
Abstract

Amnesia is a key component of Alzheimer's disease (AD) and the most important feature of its clinical diagnosis but its specificity has recently been challenged. This study investigated the ability of amnesia to predict AD in a clinicopathological dementia series. Ninety-one patients to which free and cued verbal memory assessment was administered during early cognitive decline, were followed until autopsy. Patients' histological diagnoses were classified as pure AD, mixed AD, and non-AD pathologies. Data-driven automated classification procedures explored the correspondence between memory performance and pathological diagnoses. Classifications revealed 3 clusters of performance reflecting different levels of amnesia. Little correspondence between these clusters and the presence of AD pathology was retrieved. A third of patients with pure/mixed AD pathology were non-amnesic at presentation and ≈45% of patients without AD pathology were amnesic. Data-driven prediction of AD pathology based on memory also had a poor accuracy. Free and cued memory assessments are fair tools to diagnose an amnesic syndrome but lack accuracy to predict AD pathology.

Published
2020
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15. Diagnostic positif et étiologique des démences frontotemporales

Author

Melanie Leroy, Florence Lebert, Florence Pasquier, Vincent Deramecourt, Maxime Bertoux, Thibaud Lebouvier, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U1172 Inserm - U837 (JPArc), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Université de Lille, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 (JPArc), Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Troubles cognitifs dégénératifs et vasculaires - U 1171 - EA 1046 (TCDV), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)

Subjects
03 medical and health sciences, 0302 clinical medicine, [SDV]Life Sciences [q-bio], 030212 general & internal medicine, Neurology (clinical), 030217 neurology & neurosurgery, 3. Good health
Abstract

Resume Le diagnostic positif et etiologique de la variante comportementale des degenerescences lobaires frontotemporales (DLFT), egalement appele demence frontotemporale (DFTc), reste une gageure en 2019. Le diagnostic differentiel entre DFTc et troubles psychiatriques peut etre aide par l’utilisation stricte des criteres diagnostiques du DSM5 et quelques astuces semiologiques. Le diagnostic differentiel avec les presentations executives/comportementales de maladie d’Alzheimer (MA) est egalement difficile car les troubles de la memoire episodiques sont frequents dans la DFTc. En outre les biomarqueurs de MA du liquide cerebrospinal peuvent etre positifs en cas de co-pathologie ou faussement positifs dans certaines DFTc. Enfin le diagnostic etiologique des presentations cliniques de DFTc, qui peuvent correspondre a de multiples pathologies appartenant ou non au spectre des DLFT, est particulierement difficile. Du fait de leur frequence, la recherche de mutations GRN ou C9orf72 devrait etre proposee dans tous les cas de DFTc ; la recherche de mutations plus rares peut etre reservee aux cas precoces ou familiaux. Dans les cas sporadiques, certains phenotypes clinico-radiologiques associes aux DFTc doivent etre bien connus car predictifs de la pathologie sous-jacente, comme l’association a une pathologie motoneuronale dans les DFTc liees a une DLFT-TDP de type B. L’avenir verra le developpement de marqueurs cliniques, biologiques ou d’imagerie pour ameliorer les correlations clinicopathologiques et ouvrir la voie aux essais therapeutiques de traitements neuroprotecteurs.

Published
2019
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16. Phénotypes cliniques associés aux hésitations diagnostiques entre maladie d’Alzheimer et dégénérescence lobaire frontotemporale

Author

Thibaud Lebouvier, Marie-Anne Mackowiak, Pasquier Florence, Rollin-Sillaire Adeline, Simon Lecerf, Vincent Deramecourt, and Florence Lebert

Subjects
Neurology, Neurology (clinical)
Abstract

Introduction Les degenerescences lobaires frontotemporales (DLFT) sont un groupe de pathologies heterogenes dont les presentations cliniques peuvent etre similaires a celles de la maladie d’Alzheimer (MA), ce qui est source d’hesitation diagnostique. Objectifs Le but de cette etude est de determiner les phenotypes cliniques ayant entraine une hesitation entre un diagnostic de DLFT et de MA dans une population au diagnostic final certain (par analyse histologique ou confirmation genetique). Patients et methodes Les cas etudies sont selectionnes parmi les patients ayant consulte au centre memoire de Lille ou de Bailleul entre 1993 et 2019 avec un diagnostic final certain de DLFT ou de MA. Ils sont repartis en quatre groupes : les groupes DLFT-MA et MA-DLFT (hesitation entre DLFT et MA avec respectivement diagnostic final certain de MA et de DLFT) et les groupes MA-MA et DLFT-DLFT (diagnostic sans hesitation respectivement de MA et de DLFT). Un phenotype clinique est attribue aux cas et les prevalences des differents phenotypes sont comparees. Resultats Cent vingt-neuf patients ont ete inclus dans cette etude. La prevalence des phenotypes « aphasie primaire progressive » et « presentation amnesique isolee » est significativement plus importante dans le groupe MA-DLFT (respectivement 33,3 % et 16,7 %) que dans le groupe DLFT-DLFT (respectivement 10,9 % et 0 %). La prevalence du phenotype « aphasie primaire progressive » est significativement plus importante dans le groupe DLFT-MA (47,1 %) que dans le groupe MA-MA (2,9 %). Discussion Les presentations amnesiques isolees (et de maniere plus large, les presentations comportementales avec troubles mnesiques associes) de DLFT sont source d’hesitation diagnostique avec la MA. Les presentations langagieres, notamment quand le sous-type est indetermine, peuvent egalement entrainer une hesitation entre DLFT et MA. Conclusion Dans certaines presentations cliniques, le diagnostic de DLFT et de MA reste difficile. Les prelevements cerebraux post-mortem doivent ainsi etre encourages afin de pouvoir realiser des etudes clinicopathologiques.

Published
2021
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17. A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

Author

van der Lee, Sven J, Conway, Olivia J, Jansen, Iris, Carrasquillo, Minerva M, Kleineidam, Luca, van den Akker, Erik, Hernández, Isabel, van Eijk, Kristel R, Stringa, Najada, Chen, Jason A, Zettergren, Anna, Andlauer, Till F M, Diez-Fairen, Monica, Simon-Sanchez, Javier, Lleó, Alberto, Zetterberg, Henrik, Nygaard, Marianne, Blauwendraat, Cornelis, Savage, Jeanne E, Mengel-From, Jonas, Moreno-Grau, Sonia, Wagner, Michael, Fortea, Juan, Keogh, Michael J, Blennow, Kaj, Skoog, Ingmar, Friese, Manuel A, Pletnikova, Olga, Zulaica, Miren, Lage, Carmen, de Rojas, Itziar, Riedel-Heller, Steffi, Illán-Gala, Ignacio, Wei, Wei, Jeune, Bernard, Orellana, Adelina, Then Bergh, Florian, Wang, Xue, Hulsman, Marc, Beker, Nina, Tesi, Niccolo, Morris, Christopher M, Indakoetxea, Begoña, Collij, Lyduine E, Scherer, Martin, Morenas-Rodríguez, Estrella, Ifgc, Raffaele, Ferrari, Hernandez, Dena G., Nalls, Michael A., Rohrer, Jonathan D., Adaikalavanramasamy, Kwok, John B. J., Carol, Dobson-Stone, Brooks, William S., Schofield, Peterr., Halliday, Glenda M., Hodges, John R., Olivier, Piguet, Laurenbartley, Elizabeth, Thompson, Eric, Haan, Isabel, Hernández, Agustín, Ruiz, Mercè, Boada, Barbara, Borroni, Alessandro, Padovani, Carlos, Cruchaga, Cairns, Nigel J., Luisa, Benussi, Giuliano, Binetti, Roberta, Ghidoni, Gianluigiforloni, Daniela, Galimberti, Chiara, Fenoglio, Maria, Serpente, Elio, Scarpini, Jordi, Clarimón, Alberto, Lleó, Rafael, Blesa, Maria Landqvist Waldö, Karinnilsson, Christer, Nilsson, Mackenzie, Ian R. A., Hsiung, Ging-Yuek R., Mann, DavidM. A., Jordan, Grafman, Morris, Christopher M., Johannes, Attems, Griffiths, Timothy D., Mckeith, Ian G., Thomas, Alan J., Pietrini, P., Huey, Edward D., Wassermann, Eric M., Atik, Baborie, Evelyn, Jaros, Tierney, Michael C., Pau, Pastor, Cristina, Razquin, Sara, Ortega-Cubero, Elena, Alonso, Robertperneczky, Janine, Diehl-Schmid, Panagiotis, Alexopoulos, Alexander, Kurz, Rainero, Innocenzo, Rubino, Elisa, Pinessi, Lorenzo, Ekaterina, Rogaeva, George-Hyslop, Peterst., Giacomina, Rossi, Fabrizio, Tagliavini, Giorgio, Giaccone, Rowe, James B., Schlachetzki, Johannes C. M., James, Uphill, John, Collinge, Simon, Mead, Adrian, Danek, Van Deerlin, Vivianna M., Murray, Grossman, Trojanowski, John Q., Julie van der Zee, William, Deschamps, Tim, Vanlangenhove, Marc, Cruts, Christine Van Broeckhoven, Cappa, Stefano F., Isabelle Le Ber, Didier, Hannequin, Véronique, Golfier, Martine, Vercelletto, Alexis, Brice, Benedetta, Nacmias, Sandro, Sorbi, Silvia, Bagnoli, Irene, Piaceri, Nielsen, Jørgen E., Hjermind, Lena E., Matthias, Riemenschneider, Manuelmayhaus, Bernd, Ibach, Gilles, Gasparoni, Sabrina, Pichler, Wei, Gu, Rossor, Martin N., Fox, Nick C., Warren, Jason D., Maria Grazia Spillantini, Morris, Huw R., Patrizia, Rizzu, Peter, Heutink, Snowden, Julie S., Sara, Rollinson, Annarichardson, Alexander, Gerhard, Bruni, Amalia C., Raffaele, Maletta, Fran-cesca, Frangipane, Chiara, Cupidi, Livia, Bernardi, Maria, Anfossi, Maura, Gallo, Maria Elena Conidi, Nicoletta, Smirne, Rosa, Rademakers, Matt, Baker, Dickson, Dennis W., Graff-Radford, Neill R., Petersen, Ronald C., Davidknopman, Josephs, Keith A., Boeve, Bradley F., Parisi, Joseph E., Seeley, William W., Miller, Bruce L., Karydas, Anna M., Howard, Rosen, Vanswieten, John C., Dopper, Elise G. P., Harro, Seelaar, Pijnenburg, Yolande A. L., Philipscheltens, Giancarlo, Logroscino, Rosa, Capozzo, Valeria, Novelli, Puca, Annibale A., Massimo, Franceschi, Alfredo, Postiglione, Graziella, Milan, Paolosorrentino, Mark, Kristiansen, Huei-Hsin, Chiang, Caroline, Graff, Florencepasquier, Adeline, Rollin, Vincent, Deramecourt, Florence, Lebert, Dimitrioskapogiannis, Luigi, Ferrucci, Stuart, Pickering-Brown, Singleton, Andrew B., John, Hardy, Parastoo, Momeni, Ironside, James W, van Berckel, Bart N M, Alcolea, Daniel, Wiendl, Heinz, Strickland, Samantha L, Pastor, Pau, Rodríguez Rodríguez, Eloy, Boeve, Bradley F, Petersen, Ronald C, Ferman, Tanis J, van Gerpen, Jay A, Reinders, Marcel J T, Uitti, Ryan J, Tárraga, Lluís, Maier, Wolfgang, Dols-Icardo, Oriol, Kawalia, Amit, Dalmasso, Maria Carolina, Boada, Mercè, Zettl, Uwe K, van Schoor, Natasja M, Beekman, Marian, Allen, Mariet, Masliah, Eliezer, de Munain, Adolfo López, Pantelyat, Alexander, Wszolek, Zbigniew K, Ross, Owen A, Dickson, Dennis W, Graff-Radford, Neill R, Knopman, David, Rademakers, Rosa, Lemstra, Afina W, Pijnenburg, Yolande A L, Scheltens, Philip, Gasser, Thomas, Chinnery, Patrick F, Hemmer, Bernhard, Huisman, Martijn A, Troncoso, Juan, Moreno, Fermin, Nohr, Ellen A, Sørensen, Thorkild I A, Heutink, Peter, Sánchez-Juan, Pascual, Posthuma, Danielle, Clarimón, Jordi, Christensen, Kaare, Ertekin-Taner, Nilüfer, Scholz, Sonja W, Ramirez, Alfredo, Ruiz, Agustín, Slagboom, Eline, van der Flier, Wiesje M, Holstege, Henne, Complex Trait Genetics, Amsterdam Neuroscience - Complex Trait Genetics, Sociology, The Social Context of Aging (SoCA), Universidad de Cantabria, DESGESCO Dementia Genetics, EADB Alzheimer Dis European, IFGC Int FTD-Genomics, IPDGC Int Parkinson Dis Genomics, RiMod-FTD Risk Modifying, Netherlands Brain Bank NBB, GIFT Genetic Invest, van der Lee, Sven J [0000-0003-1606-8643], Andlauer, Till FM [0000-0002-2917-5889], Tesi, Niccolo [0000-0002-1413-5091], Scheltens, Philip [0000-0002-1046-6408], Holstege, Henne [0000-0002-7688-3087], Apollo - University of Cambridge Repository, Amsterdam Neuroscience - Neurodegeneration, Neurology, Epidemiology and Data Science, Radiology and nuclear medicine, Other Research, Divisions, APH - Societal Participation & Health, APH - Aging & Later Life, Human genetics, Amsterdam Reproduction & Development (AR&D), APH - Personalized Medicine, and APH - Methodology

Subjects
0301 basic medicine, Parkinson's disease, Dementia with Lewy bodies, genetics [Alzheimer Disease], Disease, metabolism [Microglia], Bioinformatics, Neurodegenerative disease, 0302 clinical medicine, genetics [Lewy Body Disease], pathology [Brain], genetics [Parkinson Disease], Missense mutation, genetics [Frontotemporal Dementia], ALZHEIMER’S DISEASE, Brain, Parkinson Disease, purl.org/becyt/ford/3.1 [https], Alzheimer's disease, Phospholipase C Gamma 2, Biobank, 3. Good health, genetics [Amyotrophic Lateral Sclerosis], genetics [Phospholipase C gamma], purl.org/becyt/ford/3 [https], immunology [Brain], Microglia, Alzheimer’s disease, Amyotrophic lateral sclerosis, Frontotemporal dementia, Longevity, Multiple sclerosis, PLCG2, Parkinson’s disease, Progressive supranuclear palsy, Lewy Body Disease, Risk, education, Neuroimaging, Pathology and Forensic Medicine, PARKINSON’S DISEASE, 03 medical and health sciences, Cellular and Molecular Neuroscience, SDG 3 - Good Health and Well-being, Alzheimer Disease, genetics [Dementia], medicine, Humans, Genetic Predisposition to Disease, ddc:610, Alleles, Original Paper, Phospholipase C gamma, business.industry, genetics [Multiple Sclerosis], medicine.disease, 030104 developmental biology, metabolism [Brain], Mutation, Dementia, Human medicine, Neurology (clinical), business, 030217 neurology & neurosurgery, genetics [Longevity], Genome-Wide Association Study
Abstract

ATENCIÓ: la correcció està també al DDD, cal relacionar??? https://ddd.uab.cat/record/226203 Altres ajuts: The following studies and consortia have contributed to this manuscript. Amsterdam dementia Cohort (ADC): Research of the Alzheimer center Amsterdam is part of the neurodegeneration research program of Amsterdam Neuroscience. The Alzheimer Center Amsterdam is supported by Stichting Alzheimer Nederland and Stichting VUmc fonds. The clinical database structure was developed with funding from Stichting Dioraphte. Genotyping of the Dutch case-control samples was performed in the context of EADB (European Alzheimer DNA biobank) funded by the JPco-fuND FP-829-029 (ZonMW projectnumber 733051061). 100-Plus study: We are grateful for the collaborative efforts of all participating centenarians and their family members and/or relations. This work was supported by Stichting Alzheimer Nederland (WE09.2014-03), Stichting Diorapthe, horstingstuit foundation, Memorabel (ZonMW projectnumber 733050814) and Stichting VUmc Fonds. Genotyping of the 100-Plus Study was performed in the context of EADB (European Alzheimer DNA biobank) funded by the JPco-fuND FP-829-029 (ZonMW projectnumber 733051061). German Study on Ageing, Cognition and Dementia in Primary Care Patients (AgeCoDe): This study/publication is part of the German Research Network on Dementia (KND), the German Research Network on Degenerative Dementia (KNDD; German Study on Ageing, Cognition and Dementia in Primary Care Patients; AgeCoDe), and the Health Service Research Initiative (Study on Needs, health service use, costs and health-related quality of life in a large sample of oldest-old primary care patients (85+; AgeQualiDe)) and was funded by the German Federal Ministry of Education and Research (grants KND: 01GI0102, 01GI0420, 01GI0422, 01GI0423, 01GI0429, 01GI0431, 01GI0433, 01GI0434; grants KNDD: 01GI0710, 01GI0711, 01GI0712, 01GI0713, 01GI0714, 01GI0715, 01GI0716; grants Health Service Research Initiative: 01GY1322A, 01GY1322B, 01GY1322C, 01GY1322D, 01GY1322E, 01GY1322F, 01GY1322G). Alfredo Ramirez was partly supported by the ADAPTED consortium: Alzheimer's disease Apolipoprotein Pathology for Treatment Elucidation and Development, which has received funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 115975. Brain compendium: This work was funded by the UK Medical Research Council (13044). P.F.C. is a Wellcome Trust principal Fellow (212219/Z/18/Z) and a UK NIHR Senior Investigator, who receives support from the Medical Research Council Mitochondrial Biology Unit (MC_UU_00015/9), and the National Institute for Health Research (NIHR) Biomedical Research Centre based at Cambridge University Hospitals NHS Foundation Trust and the University of Cambridge. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, or the Department of Health.Clinical AD, Sweden: We would like to thank UCL Genomics for performing the genotyping analyses. Danish data: The studies behind the Danish long-lived cases received funding from The National Program for Research Infrastructure 2007 (grant no. 09-063256), the Danish Agency for Science Technology and Innovation, the Velux Foundation, the US National Institute of Health (P01 AG08761), the Danish Agency for Science, Technology and Innovation/The Danish Council for Independent Research (grant no. 11-107308), the European Union's Seventh Framework Programme (FP7/2007-2011) under grant agreement no. 259679, the INTERREG 4 A programme Syddanmark-Schleswig-K.E.R.N. (by EU funds from the European Regional Development Fund), the CERA Foundation (Lyon), the AXA Research Fund, Paris, and The Health Foundation (Helsefonden), Copenhagen, Denmark. The GOYA study was conducted as part of the activities of the Danish Obesity Research Centre (DanORC, www.danorc.dk) and The MRC centre for Causal Analyses in Translational Epidemiology (MRC CAiTE). The genotyping for GOYA was funded by the Wellcome Trust (WT 084762). GOYA is a nested study within The Danish National Birth Cohort which was established with major funding from the Danish National Research Foundation. Additional support for this cohort has been obtained from the Pharmacy Foundation, the Egmont Foundation, The March of Dimes Birth Defects Foundation, the Augustinus Foundation, and the Health Foundation. Fundació ACE (FACE): We would like to thank patients and controls who participated in this project. We are indebted to Trinitat Port-Carbó and her family for their support of Fundació ACE research programs. Fundació ACE collaborates with the Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, Spain) and is one of the participating centers of the Dementia Genetics Spanish Consortium (DEGESCO). Agustín Ruiz has received support from the EU/EFPIA Innovative Medicines Initiative Joint Undertaking ADAPTED Grant No. 115975 and by grants PI13/02434 and PI16/01861. Acción Estratégica en Salud, integrated in the Spanish National R + D + I Plan and financed by ISCIII (Instituto de Salud Carlos III)-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER- "Una manera de Hacer Europa"), by Fundación bancaria "La Caixa" and Grifols SA (GR@ACE project). Genetics of Healthy Ageing Study (GEHA - NL): The work described in this paper was funded mainly by the EU GEHA Project contract no. LSHM-CT-2004-503-270. Gothenburg Birth Cohort (GBC) Studies: We would like to thank UCL Genomics for performing the genotyping analyses. The studies were supported by The Stena Foundation, The Swedish Research Council (2015-02830, 2013-8717), The Swedish Research Council for Health, Working Life and Wellfare (2013-1202, 2005-0762, 2008-1210, 2013-2300, 2013-2496, 2013-0475), The Brain Foundation, Sahlgrenska University Hospital (ALF), The Alzheimer's Association (IIRG-03-6168), The Alzheimer's Association Zenith Award (ZEN-01-3151), Eivind och Elsa K:son Sylvans Stiftelse, The Swedish Alzheimer Foundation. International FTD-Genomics Consortium (IFGC): International FTD-Genomics Consortium (IFGC): The authors thank the IFGC for providing relevant data to support the analyses presented in this manuscript. Further acknowledgments for IFGC (https://ifgcsite.wordpress.com/), e.g. full members list and affiliations, are found in the online supplementary files. IPDGC (​The International Parkinson Disease Genomics Consortium): We also would like to thank all members of the International Parkinson Disease Genomics Consortium (IPDGC). See for a complete overview of members, acknowledgements and funding http://pdgenetics.org/partners. Kompetenznetz Multiple Sklerose (KKNMS): This work was supported by the German Ministry for Education and Research (BMBF) as part of the "German Competence Network Multiple Sclerosis" (KKNMS) (grant nos. 01GI0916 and 01GI0917) and the Munich Cluster for Systems Neurology (SyNergy). TA was supported by the BMBF through the Integrated Network IntegraMent, under the auspices of the e:Med Programme (01ZX1614J). BH was supported by the EU Horizon 2020 project MultipleMS.Longitudinal Aging Study Amsterdam (LASA) is largely supported by a grant from the Netherlands Ministry of Health, Welfare and Sports, Directorate of Long-Term Care. The authors are grateful to all LASA participants, the fieldwork team and all researchers for their ongoing commitment to the study. Leiden Longevity Study: This study was supported by a grant from the Innovation-Oriented Research Program on Genomics (SenterNovem IGE05007), the Centre for Medical Systems Biology, and the Netherlands Consortium for Healthy Ageing (Grant 050-060-810), all in the framework of the Netherlands Genomics Initiative/Netherlands Organization for Scientific Research (NWO) and by Unilever Colworth.Maria Carolina Dalmasso: Georg Forster Research Award (Alexander von Humboldt Foundation). Mayo Clinic AD, DLB, PD, PSP: We thank the patients and their families for their participation, without whom these studies would not have been possible. Funding for this work was supported by National Institute on Aging [RF AG051504 to NET.; U01 AG046139 to NET]; and National Institute of Neurological Disorders and Stroke [R01 NS080820 to NET; P50 NS072187]. The Mayo Clinic is a Lewy Body Dementia Association (LBDA) Research Center of Excellence, American Parkinson Disease Association (APDA) Information and Referral Center and Center for Advanced Research, NINDS Tau Center without Walls (U54-NS100693) and is supported by Mayo Clinic AD and related dementias genetics program, The Little Family Foundation, the Mangurian Foundation for Lewy body research and NINDS R01 NS078086 (to OAR). The PD program at the Mayo Clinic Florida is also supported by the Mayo Clinic Center for Regenerative Medicine, Mayo Clinic Center for Individualized Medicine, Mayo Clinic Neuroscience Focused Research Team (Cecilia and Dan Carmichael Family Foundation, and the James C. and Sarah K. Kennedy Fund for Neurodegenerative Disease Research at Mayo Clinic in Florida), the gift from Carl Edward Bolch, Jr., and Susan Bass Bolch, and The Sol Goldman Charitable Trust. Samples included in this study are from the brain bank at Mayo Clinic in Jacksonville which is supported by CurePSP The online version of this article (10.1007/s00401-019-02026-8) contains supplementary material, which is available to authorized users.

Published
2019
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18. Integrative system biology analyses of CRISPR-edited iPSC-derived neurons and human brains reveal deficiencies of presynaptic signaling in FTLD and PSP

Author

Jiang, Shan, Wen, Natalie, Zeran, Li, Dube, Umber, Del Aguila, Jorge, Budde, John, Martinez, Rita, Hsu, Simon, Fernandez, Maria V, Cairns, Nigel J, Harari, Oscar, Cruchaga, Carlos, Karch, Celeste MRaffaele Ferrari, Dena, G Hernandez, Michael, A Nalls, Jonathan, D Rohrer, Adaikalavan, Ramasamy, John B, J Kwok, Carol, Dobson-Stone, William, S Brooks, Peter, R Schofield, Glenda, M Halliday, John, R Hodges, Olivier, Piguet, Lauren, Bartley, Elizabeth, Thompson, Eric, Haan, Isabel, Hernández, Agustín, Ruiz, Mercè, Boada, Barbara, Borroni, Alessandro, Padovani, Carlos, Cruchaga, Nigel, J Cairns, Luisa, Benussi, Giuliano, Binetti, Roberta, Ghidoni, Gianluigi, Forloni, Daniela, Galimberti, Chiara, Fenoglio, Maria, Serpente, Elio, Scarpini, Jordi, Clarimón, Alberto, Lleó, Rafael, Blesa, Maria Landqvist Waldö, Karin, Nilsson, Christer, Nilsson, Ian R, A Mackenzie, Ging-Yuek, R Hsiung, David M, A Mann, Jordan, Grafman, Christopher, M Morris, Johannes, Attems, Timothy, D Griffiths, Ian, G McKeith, Alan, J Thomas, Pietrini, P, Edward, D Huey, Eric, M Wassermann, Atik, Baborie, Evelyn, Jaros, Michael, C Tierney, Pau, Pastor, Cristina, Razquin, Sara, Ortega-Cubero, Elena, Alonso, Robert, Perneczky, Janine, Diehl-Schmid, Panagiotis, Alexopoulos, Alexander, Kurz, Rainero, Innocenzo, Rubino, Elisa, Lorenzo, Pinessi, Ekaterina, Rogaeva, Peter St George-Hyslop, Giacomina, Rossi, Fabrizio, Tagliavini, Giorgio, Giaccone, James, B Rowe, Johannes C, M Schlachetzki, James, Uphill, John, Collinge, Simon, Mead, Adrian, Danek, Vivianna, M Van Deerlin, Murray, Grossman, John, Q Trojanowski, Julie van der Zee, William, Deschamps, Tim Van Langenhove, Marc, Cruts, Christine Van Broeckhoven, Stefano, F Cappa, Isabelle Le Ber, Didier, Hannequin, Véronique, Golfier, Martine, Vercelletto, Alexis, Brice, Benedetta, Nacmias, Sandro, Sorbi, Silvia, Bagnoli, Irene, Piaceri, Jørgen, E Nielsen, Lena, E Hjermind, Matthias, Riemenschneider, Manuel, Mayhaus, Bernd, Ibach, Gilles, Gasparoni, Sabrina, Pichler, Wei, Gu, Martin, N Rossor, Nick, C Fox, Jason, D Warren, Maria Grazia Spillantini, Huw, R Morris, Patrizia, Rizzu, Peter, Heutink, Julie, S Snowden, Sara, Rollinson, Anna, Richardson, Alexander, Gerhard, Amalia, C Bruni, Raffaele, Maletta, Francesca, Frangipane, Chiara, Cupidi, Livia, Bernardi, Maria, Anfossi, Maura, Gallo, Maria Elena Conidi, Nicoletta, Smirne, Rosa, Rademakers, Matt, Baker, Dennis, W Dickson, Neill, R Graff-Radford, Ronald, C Petersen, David, Knopman, Keith, A Josephs, Bradley, F Boeve, Joseph, E Parisi, William, W Seeley, Bruce, L Miller, Anna, M Karydas, Howard, Rosen, John, C van Swieten, Elise G, P Dopper, Harro, Seelaar, Yolande A, L Pijnenburg, Philip, Scheltens, Giancarlo, Logroscino, Rosa, Capozzo, Valeria, Novelli, Annibale, A Puca, Massimo, Franceschi, Alfredo, Postiglione, Graziella, Milan, Paolo, Sorrentino, Mark, Kristiansen, Huei-Hsin, Chiang, Caroline, Graff, Florence, Pasquier, Adeline, Rollin, Vincent, Deramecourt, Florence, Lebert, Dimitrios, Kapogiannis, Luigi, Ferrucci, Stuart, Pickering-Brown, Andrew, B Singleton, John, Hardy, and Parastoo, Momeni

Subjects
0301 basic medicine, Male, Tau protein, Induced Pluripotent Stem Cells, tau Proteins, medicine.disease_cause, Article, lcsh:RC321-571, Progressive supranuclear palsy, 03 medical and health sciences, Cellular and Molecular Neuroscience, Receptors, GABA, medicine, Animals, Humans, Induced pluripotent stem cell, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Biological Psychiatry, Aged, Aged, 80 and over, Neurons, Mutation, biology, Brain, Frontotemporal lobar degeneration, Human brain, medicine.disease, 3. Good health, Cell biology, Mice, Inbred C57BL, Psychiatry and Mental health, 030104 developmental biology, medicine.anatomical_structure, biology.protein, Female, Tauopathy, Supranuclear Palsy, Progressive, CRISPR-Cas Systems, Frontotemporal Lobar Degeneration, Transcriptome, Frontotemporal dementia, Signal Transduction
Abstract

Mutations in the microtubule-associated protein tau (MAPT) gene cause autosomal dominant frontotemporal lobar degeneration with tau inclusions (FTLD-tau). MAPT p.R406W carriers present clinically with progressive memory loss and neuropathologically with neuronal and glial tauopathy. However, the pathogenic events triggered by the expression of the mutant tau protein remain poorly understood. To identify the genes and pathways that are dysregulated in FTLD-tau, we performed transcriptomic analyses in induced pluripotent stem cell (iPSC)–derived neurons carrying MAPT p.R406W and CRISPR/Cas9-corrected isogenic controls. We found that the expression of the MAPT p.R406W mutation was sufficient to create a significantly different transcriptomic profile compared with that of the isogeneic controls and to cause the differential expression of 328 genes. Sixty-one of these genes were also differentially expressed in the same direction between MAPT p.R406W carriers and pathology-free human control brains. We found that genes differentially expressed in the stem cell models and human brains were enriched for pathways involving gamma-aminobutyric acid (GABA) receptors and pre-synaptic function. The expression of GABA receptor genes, including GABRB2 and GABRG2, were consistently reduced in iPSC-derived neurons and brains from MAPT p.R406W carriers. Interestingly, we found that GABA receptor genes, including GABRB2 and GABRG2, are significantly lower in symptomatic mouse models of tauopathy, as well as in brains with progressive supranuclear palsy. Genome wide association analyses reveal that common variants within GABRB2 are associated with increased risk for frontotemporal dementia (P −3). Thus, our systems biology approach, which leverages molecular data from stem cells, animal models, and human brain tissue can reveal novel disease mechanisms. Here, we demonstrate that MAPT p.R406W is sufficient to induce changes in GABA-mediated signaling and synaptic function, which may contribute to the pathogenesis of FTLD-tau and other primary tauopathies.

Published
2018

19. The Swiss Household Panel Study: Observing social change since 1999

Author

Robin Tillmann, Marieke Voorpostel, Boris Wernli, Erika Antal, Ursina Kuhn, Oliver Lipps, Florence Lebert, and Valérie-Anne Ryser

Subjects
Longitudinal study, Data collection, Geography, Longitudinal data, 05 social sciences, Social change, 050602 political science & public administration, 050109 social psychology, 0501 psychology and cognitive sciences, Sample (statistics), Life-span and Life-course Studies, Socioeconomics, 0506 political science
Abstract

Collecting data on households and individuals since 1999, the Swiss Household Panel (SHP) is an ongoing, unique, large-scale, nationally representative, longitudinal study in Switzerland (N=7,383 households and N=12,119 persons interviewed in 2014). The data of the SHP provide a rich source of information to study social change in Switzerland over a significant period on a wide variety of topics. The SHP aims to provide both continuity and innovation in measurement and data collection, with the combination of retrospective and prospective longitudinal data in the most recent refreshment sample as one notable example of such an innovation. This paper provides an overview of the SHP – focusing on its origin, aims, design, content, data collection and adjustments, possibilities for cross-national comparisons, data use and accomplishments.

Published
2016
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20. Detection of Cortical Microbleeds in Postmortem Brains of Patients with Lewy Body Dementia: A 7.0-Tesla Magnetic Resonance Imaging Study with Neuropathological Correlates

Author

Didier Leys, Claude-Alain Maurage, Florent Auger, Charlotte Cordonnier, Florence Lebert, Florence Pasquier, Jacques De Reuck, Vincent Deramecourt, Nicolas Durieux, and Régis Bordet

Subjects
Lewy Body Disease, Male, Pathology, medicine.medical_specialty, animal structures, Autopsy, mental disorders, medicine, Humans, Dementia, Aged, Cerebral Hemorrhage, Cerebrovascular pathology, Aged, 80 and over, Lewy body, medicine.diagnostic_test, fungi, Magnetic resonance imaging, Middle Aged, medicine.disease, Magnetic Resonance Imaging, Hyperintensity, Frontal Lobe, Neurology, Frontal lobe, Female, Neurology (clinical), Cerebral amyloid angiopathy, Psychology, Neuroscience, hormones, hormone substitutes, and hormone antagonists
Abstract

Background: It is unclear whether associated cerebrovascular pathology contributes to the clinical spectrum of Lewy body dementia (LBD). Summary: The present postmortem 7.0-tesla MRI study investigates the anatomical distribution of cortical microbleeds (CoMBs) in LBD brains with and without associated Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA). CoMBs predominated in the frontal section of the LBD brains and were associated to severe white matter lesions. No differences were observed when LBD brains with and without AD and CAA were compared. Key Messages: In LBD, there is a specific distribution of CoMBs that is different from that in other neurodegenerative diseases. The increase of frontal CoMBs is not due to the frequently associated AD and CAA features but due to the LBD itself.

Published
2015
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21. Frontotemporal Dementia

Author

Florence Pasquier, Thibaud Lebouvier, and Florence Lebert

Subjects
03 medical and health sciences, 0302 clinical medicine, 030212 general & internal medicine, 030217 neurology & neurosurgery
Published
2016
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22. Attrition when dropping CAPI from a CATI/CAPI panel survey

Author

Florence Lebert and Oliver Lipps

Subjects
Panel survey, First language, 05 social sciences, 050401 social sciences methods, Advertising, Mixed mode, medicine.disease, 01 natural sciences, 010104 statistics & probability, 0504 sociology, medicine, Attrition, Demographic economics, Landline, 0101 mathematics, Psychology, Residence permit
Abstract

In this paper, we study attrition in a household panel survey, where in the first wave those with a matched landline number were surveyed by telephone, while those without received a face-to-face visit. In the second wave, the face-to-face mode was dropped. We find among the first wave face-to-face households a high likelihood to attrite due to "no contact" rather than due to "cannot be tracked" or "refusal". Socio-demographic characteristics have the expected effects. For example households with young children, with a short-term residence permit, or one-person households cannot be tracked, while those with a face-to-face visit in the first wave, or foreigners with a mother tongue that is not offered in the survey refuse more often. More first wave calls and contacts are associated with all reasons to attrite, in particular with refusal. Based on the findings, we give recommendations to tailor fieldwork to decrease attrition.

Published
2016

23. Young onset demented patients in French cognitive-behavioral specialized units

Author

Melanie Leroy, Florence Lebert, Florence Pasquier, and Denise Strubel

Subjects
Male, Yod, medicine.medical_specialty, medicine.medical_treatment, Disease, Psychiatric Department, Hospital, Alzheimer Disease, medicine, Humans, Age of Onset, Biological Psychiatry, Cognitive Behavioral Therapy, business.industry, Cognition, Caregiver burden, Middle Aged, medicine.disease, Neuropsychology and Physiological Psychology, Family medicine, Frontotemporal Dementia, Cognitive therapy, Female, Neurology (clinical), France, Geriatrics and Gerontology, Age of onset, Alzheimer's disease, business, Hospital Units, Frontotemporal dementia
Abstract

The number of patients with young onset dementia (YOD) (first symptoms beginning before the age of 60 years) is estimated around 5,000 in France. On account of the usual severity of behavioral symptoms in these patients, the need for cognitive-behavioral specialized unit (UCC) is expected. To determine the number and characteristics of YOD patients cared for in UCC in France during the year 2013. A specific questionnaire was sent to the 84 French UCC. The questionnaire was completed by 55 UCC (65%), whose 33 received 179 YOD patients. The diagnosis was Alzheimer's disease in 50% of the cases and frontotemporal dementia in 30%. The main reasons for the hospitalization in UCC were the severity of behavioral symptoms in 86% of cases, the need to alleviate the caregiver burden in 31% and the waiting for a place in a nursing home in 23%. Mean duration of hospitalization was 40.4 ± 20.5 days. At the end of hospitalization 51% of the patients returned to their original living accomodation and 39% entered into a nursing home. The main reason of YOD patients hospitalization reject was the care team's fear in the UCC without experience. The severity of the behavioral troubles was the major issue while the necessary ethical reflection raised by the YOD patients management was a positive aspect. The teams rated how ready do they feel about taking care of YOD patients on a scale from 0 to 100, the median was 35. The welcoming of YOD patients in UCC is necessary, however the severity of the behavioral troubles and the care teams fear prompt to set up specific education and to increase of the number of staff for YOD patients management.

Published
2016

24. My belief or yours? Differential theory of mind deficits in frontotemporal dementia and Alzheimer’s disease

Author

Florence Lebert, Franck Semah, P. Lenfant, Xavier Delbeuck, Laura Ravasi, Florence Pasquier, and Raphaël Le Bouc

Subjects
Cerebral Cortex, Male, Temporoparietal junction, Theory of Mind, Neuropsychology, Cognition, Middle Aged, Neuropsychological Tests, medicine.disease, Executive functions, medicine.anatomical_structure, Alzheimer Disease, Fluorodeoxyglucose F18, Frontotemporal Dementia, Theory of mind, medicine, Humans, Neurology (clinical), Alzheimer's disease, Psychology, Aged, Stroop effect, Frontotemporal dementia, Cognitive psychology
Abstract

Theory of mind reasoning-the ability to understand someone else's mental states, such as beliefs, intentions and desires-is crucial in social interaction. It has been suggested that a theory of mind deficit may account for some of the abnormalities in interpersonal behaviour that characterize patients affected by behavioural variant frontotemporal dementia. However, there are conflicting reports as to whether understanding someone else's mind is a key difference between behavioural variant frontotemporal dementia and other neurodegenerative conditions such as Alzheimer's disease. Literature data on the relationship between theory of mind abilities and executive functions are also contradictory. These disparities may be due to underestimation of the fractionation within theory of mind components. A recent theoretical framework suggests that taking someone else's mental perspective requires two distinct processes: inferring someone else's belief and inhibiting one's own belief, with involvement of the temporoparietal and right frontal cortices, respectively. Therefore, we performed a neuropsychological and neuroimaging study to investigate the hypothesis whereby distinct cognitive deficits could impair theory of mind reasoning in patients with Alzheimer's disease and patients with behavioural variant frontotemporal dementia. We used a three-option false belief task to assess theory of mind components in 11 patients with behavioural variant frontotemporal dementia, 12 patients with Alzheimer's disease and 20 healthy elderly control subjects. The patients with behavioural variant frontotemporal dementia and those with Alzheimer's disease were matched for age, gender, education and global cognitive impairment. [(18)F]-fluorodeoxyglucose-positron emission tomography imaging was used to investigate neural correlates of theory of mind reasoning deficits. Performance in the three-option false belief task revealed differential impairments in the components of theory of mind reasoning; patients with Alzheimer's disease had a predominant deficit in inferring someone else's belief, whereas patients with behavioural variant frontotemporal dementia were selectively impaired in inhibiting their own mental perspective. Moreover, inhibiting one's own perspective was strongly correlated with inhibition in a Stroop task but not with other subprocesses of executive functions. This finding suggests that self-perspective inhibition may depend on cognitive processes that are not specific to the social domain. Last, the severity of the deficit in inferring someone else's beliefs correlated significantly over all subjects with hypometabolism in the left temporoparietal junction, whereas the severity of the deficit in self-perspective inhibition correlated significantly with hypometabolism in the right lateral prefrontal cortex. In conclusion, our findings provided clinical and imaging evidence to support differential deficits in two components of theory of mind reasoning (subserved by distinct brain regions) in patients with Alzheimer's disease and patients with behavioural variant frontotemporal dementia.

Published
2012
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25. De la maladie de Pick aux démences fronto-temporales

Author

Florence Pasquier, Florence Lebert, and Vincent Deramecourt

Subjects
medicine.medical_specialty, business.industry, Environmental adaptation, General Medicine, Disease, Degeneration (medical), medicine.disease, Parkinsonian syndromes, Degenerative disease, Supranuclear palsy, mental disorders, medicine, Corticobasal degeneration, business, Psychiatry, Frontotemporal dementia
Abstract

Frontotemporal dementias (FTD) are defined by a gradual change in social conduct, behavior and language, associated with frontal and anterior temporal lobe degeneration. The clinicalfeatures depend on the location of the degenerative process. In the last 20 years, increasingly specific and sensitive operational criteria have been established. Ongoing neuropathological and genetic studies have highlighted overlaps between FTD, motor neuron disease, and atypical parkinsonian syndromes (supranuclear palsy, corticobasal degeneration). They have also provided a better knowledge of the pathophysiology of FTD, and new specific therapeutic targets. These dementias, which usually occur before the age of 65 years, are now better recognized but are still underdiagnosed and often initially mistaken for psychiatric illnesses. Healthcare professionals managing these patients must therefore be better informed Serotonergic agents provide a symptomatic improvement, but environmental adaptation, prevention of language and swallowing difficulties, and information and support for the family and caregivers remain essential.

Published
2012
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26. Alzheimer disease with cerebrovascular disease and vascular dementia: clinical features and course compared with Alzheimer disease

Author

Philippe Amouyel, Florence Pasquier, Vincent Deramecourt, Amélie Bruandet, Claude Alain Maurage, Stéphanie Bombois, Florence Richard, and Florence Lebert

Subjects
Male, medicine.medical_specialty, Neuropsychological Tests, Severity of Illness Index, Alzheimer Disease, Internal medicine, Activities of Daily Living, mental disorders, Severity of illness, Humans, Medicine, Dementia, cardiovascular diseases, Age of Onset, Cognitive decline, Vascular dementia, Aged, Demography, Mini–Mental State Examination, medicine.diagnostic_test, business.industry, Dementia, Vascular, Memory clinic, Brain, medicine.disease, Magnetic Resonance Imaging, Cerebrovascular Disorders, Psychiatry and Mental health, Hypertension, Disease Progression, Physical therapy, Female, Surgery, Neurology (clinical), Alzheimer's disease, Age of onset, Tomography, X-Ray Computed, business, Follow-Up Studies
Abstract

Vascular dementia (VaD) and Alzheimer disease with cerebrovascular disease (AD+CVD) are the leading causes of dementia after Alzheimer disease alone (AD). Little is known about the progression of either VaD or AD+CVD. The aim of this study was to compare demographic features, cognitive decline and survival of patients with VaD, AD+CVD and AD alone attending a memory clinic.This study included 970 patients who were followed at the Lille-Bailleul memory clinic, France. Cognitive functions were measured with the Mini Mental State Examination (MMSE) and the Dementia Rating Scale (DRS). Survival rate was analysed with a left-truncated Cox model. Analyses were adjusted for age, sex, education, hypertension, diabetes and baseline MMSE and DRS.Of 970 patients, 141 had VaD, 663 AD alone and 166 AD+CVD. The latter were significantly older than AD or VaD patients at onset (71 (SD 7) vs 69 (9) and 68 (9) years, p = 0.01) and at first visit (75 (6) vs 73 (8) and 72 (8) years, p = 0.0002). Baseline MMSE and DRS evaluations were highest for VaD compared with AD alone or AD+CVD patients (p0.006). Cognitive decline during follow-up was slowest for VaD, intermediate for AD+CVD and fastest for AD alone (p = 0.03). After adjustment, compared with AD patients, mortality risk was similar for those with VaD (relative mortality risk (RR) = 0.7 (0.5 to 1.1)) and tended to be lower for AD+CVD (RR = 0.7 (0.5 to 1.0)). The shorter the delay between first symptoms and first visit, the longer patients survived.This clinical cohort study shows that patients with VaD, AD+CVD and AD present different characteristics at baseline and during follow-up, and underlines the need to distinguish between them.

Published
2009
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27. Biochemical Staging of Synucleinopathy and Amyloid Deposition in Dementia With Lewy Bodies

Author

Claude Alain Maurage, Antoine Ghestem, S. Bombois, Hervé Drobecq, Vincent Deramecourt, Florence Lebert, Florence Pasquier, Eugeen Vanmechelen, André Delacourte, Neuroendocrinologie et physiopathologie neuronale, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Troubles cognitifs vasculaires et dégénératifs - EA 2691 (TCDV), Université de Lille, Droit et Santé, Synthèse, structure et fonction des biomolécules (SSFB), Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique (CNRS), INNOGENETICS N.V, This work was supported by the integrated project APOPIS (Abnormal Proteins in the Pathogenesis of Neurodegenerative Disorders) funded by the European Community under the sixth framework program., and The authors thank Innogenetics for the gift of alpha-synuclein antibody Syn1b (3B5) and recombinant alpha-synuclein.

Subjects
Male, MESH: Lewy Body Disease/pathology, Pathology, Dementia with Lewy bodies, MESH: Alzheimer Disease/pathology, [CHIM.THER]Chemical Sciences/Medicinal Chemistry, Mass Spectrometry, Amyloid beta-Protein Precursor, chemistry.chemical_compound, MESH: Aged, 80 and over, 0302 clinical medicine, MESH: alpha-Synuclein/metabolism, MESH: Parkinson Disease/metabolism, Amyloid precursor protein, Electrophoresis, Gel, Two-Dimensional, Senile plaques, MESH: Amyloid beta-Protein Precursor/metabolism, Aged, 80 and over, Cerebral Cortex, MESH: Aged, 0303 health sciences, MESH: Middle Aged, biology, MESH: Parkinson Disease/pathology, Parkinson Disease, MESH: tau Proteins/metabolism, General Medicine, Middle Aged, MESH: Cerebral Cortex/metabolism, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biomolecules [q-bio.BM], 3. Good health, Neurology, Female, Tauopathy, Alzheimer disease, Alzheimer's disease, Lewy Body Disease, Amyloid, medicine.medical_specialty, tau Proteins, Neuropathology, MESH: Cerebral Cortex/anatomy & histology, Pathology and Forensic Medicine, Alpha-synuclein, 03 medical and health sciences, Cellular and Molecular Neuroscience, mental disorders, medicine, Humans, MESH: Alzheimer Disease/metabolism, Aged, 030304 developmental biology, MESH: Mass Spectrometry, MESH: Humans, MESH: Lewy Body Disease/metabolism, business.industry, MESH: Electrophoresis, Gel, Two-Dimensional, medicine.disease, MESH: Male, nervous system diseases, chemistry, biology.protein, Neurology (clinical), MESH: Cerebral Cortex/pathology, business, MESH: Female, Biomarkers, 030217 neurology & neurosurgery
Abstract

The primary feature of dementia with Lewy bodies (DLB) is the aggregation of alpha-synuclein into characteristic lesions: Lewy bodies (LBs) and Lewy neurites. However, in most of DLB cases, LBs are associated with neurofibrillary tangles and amyloid plaques (both Alzheimer disease [AD]-related lesions). We wanted to determine if this overlap of lesions is statistical, as a result of the late onset of both diseases, or results from a specific physiopathological synergy between synucleinopathy and either tauopathy or amyloid pathology. All patients with DLB from our prospective and multidisciplinary study were analyzed. These cases were compared with cases with pure AD and patients with Parkinson disease and controls. All cases were analyzed thoroughly at the neuropathologic and biochemical levels with a biochemical staging of aggregated alpha-synuclein, tau, and Abeta species. All sporadic cases of DLB were associated with abundant deposits of Abeta x-42 that were similar in quality and quantity to those of AD. Amyloid precursor protein (APP) dysfunction is a risk factor for AD as demonstrated by pathogenic mutations and Abeta accumulation. The constant and abundant Abeta x-42 deposition in sporadic DLB suggests that synucleinopathy is also promoted by APP dysfunction. Therefore, we conclude that APP is a therapeutic target for both AD and DLB.

Published
2006
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28. Behavioral benefits of trazodone are sustained for the long term in frontotemporal dementia

Author

Florence Lebert

Subjects
medicine.medical_specialty, Pediatrics, business.industry, Extension study, Trazodone, General Medicine, medicine.disease, Neuropsychiatric inventory, Withdrawal rate, medicine, Dementia, Pharmacology (medical), Cognitive decline, Psychiatry, business, Adverse effect, Frontotemporal dementia, medicine.drug
Abstract

Objective: Previously, a placebo-controlled cross-over trial of trazodone (300 mg/day) of 12-weeks duration showed behavioral improvement in a group of 26 patients with frontotemporal dementia. The long-term efficacy and safety of trazodone in frontotemporal dementia was unknown. Materials & methods: The placebo-controlled trial has now been followed by an open-label extension study. The 26 frontotemporal dementia patients with mild cognitive decline and severe behavioral troubles who entered the study had previously completed the double-blind study with trazodone. Patients were treated with 300 mg/day. They were followed for at least 2 years, after the end of the double-blind trial. The efficacy was evaluated by the neuropsychiatric inventory score. Results: The withdrawal rate was approximately 23% during the first year, two patients died due to unrelated causes, two patients were institutionalized and two refused the follow-up – none as a result of adverse events. The withdrawal rate was approximately ...

Published
2006
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29. Consensus sur la démence de type Alzheimer au stade sévère

Author

Jean-Louis Montastruc, Philippe Robert, Jean-Pierre Aquino, Jacques Touchon, François Blanchard, Marc Verny, Fati Nourhashemi, A. Franco, Jean-Francois Dartigues, Pierre-Jean Ousset, Sandrine Andrieu, Denise Strubel, Geneviève Ruault, Vincent Camus, Jérémie Pariente, Marie-Eve Joel, Bruno Vellas, Bruno Dubois, Serge Gauthier, Alain Grand, Françoise Forette, Claude Jeandel, Pierre Jouanny, J.-M. Vetel, Hervé Allain, Régis Gonthier, Marie-Pierre Hervy, Gilles Berrut, Anne-Sophie Rigaud, P. Michot, M. Berthel, and Florence Lebert

Subjects
Geriatrics, medicine.medical_specialty, Public health, MEDLINE, Disease, medicine.disease, Neurology, Severe dementia, Family medicine, Severity of illness, medicine, Dementia, Neurology (clinical), Alzheimer's disease, Psychiatry, Psychology
Abstract

Under the auspices of the French Society of Gerontology and Geriatrics, a multidisciplinary team including geriatritians, neurologists, epidemiologists, psychiatrists, pharmacologists and public health specialists developed a consensus on care for patients with severe dementia. They defined 21 recommendations for general practitioners, long-term care physicians and specialists based on knowledge available in 2005. At all stages of the disease, the objective of care is to improve as much as possible quality-of-life for the patient and his/her family, including a life project until the end of life. It is always possible to do something for these patients and their family: nutritional status, behavior disorders, and incapacities to deal with basic activities of daily life have to be taken in consideration. Resource allocation and proximity care have to be targeted. Research areas necessary to improve the care of patients with severe dementia has been selected.

Published
2005
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30. Natural History of Frontotemporal Dementia: Comparison with Alzheimer’s Disease

Author

Florence Richard, Florence Pasquier, and Florence Lebert

Subjects
Adult, Male, medicine.medical_specialty, Time Factors, Cognitive Neuroscience, Disease, Neuropsychological Tests, Risk Assessment, Alzheimer Disease, Cause of Death, mental disorders, Confidence Intervals, medicine, Humans, Dementia, Psychiatry, Natural course, Disease progression, nutritional and metabolic diseases, Middle Aged, medicine.disease, Survival Analysis, nervous system diseases, Natural history, Psychiatry and Mental health, Multicenter study, Disease Progression, Female, Geriatrics and Gerontology, Alzheimer's disease, Psychology, Frontotemporal dementia
Abstract

Introduction: Frontotemporal dementia (FTD) is a more common cause of dementia than previously recognised. Few data are available regarding the natural course of FTD in terms of survival, nursing home admission and causes of death. Methods: An observational study of all consecutive patients referred to the memory centre of Lille, France, between 1995 and 1999, and examined at least twice in this centre, with a diagnosis of FTD (frontal or behavioural variant) or of Alzheimer’s disease (AD) was performed. Kaplan-Meyer analysis allowing for delayed entry was used to compare the survival functions in FTD and AD. Results: 552 patients were included, of whom 49 (8.9%) were lost to follow-up at 3 years. FTD patients were younger (mean age at onset 59 years), had more often a family history of psychiatric disorders (20%), had a longer delay between first symptoms and first visit (5.9 years) and a higher Mini-Mental State Examination (MMSE) score at first visit (24.5) than patients with AD (19.9). The mean annual MMSE score decline was 0.9 point in FTD vs. 2.0 points in AD (p < 0.0004). Fewer patients with FTD than with AD entered an institution (RR: 0.20, 95% CI 0.05–0.81). After adjustment for sex, age at first visit, level of education and MMSE score at first visit, survival rates in FTD and AD did not differ significantly. Patients with FTD often had a sudden death, the cause of which could not be found. The earlier the first visit after onset, the longer the survival rate, whatever the diagnosis (RR: 0.76, 95% CI 0.67–0.86, p < 0.0001 per year of earlier first visit). Conclusion: This large study showed that the mean duration of FTD was 2 years longer than that of AD, but the risk of death after adjustment for age and sex was similar in FTD and in AD. Sudden and unexplained causes of death were frequent and need further study. Early management increases the life span of demented patients.

Published
2004
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31. Influence of prestroke dementia on early and delayed mortality in stroke patients

Author

Isabelle Durieu, Hilde Hénon, Didier Leys, Florence Pasquier, and Florence Lebert

Subjects
Adult, Pediatrics, medicine.medical_specialty, Time Factors, Neurology, Comorbidity, Fibrinolytic Agents, Risk Factors, Informant Questionnaire on Cognitive Decline in the Elderly, Prevalence, medicine, Humans, Dementia, Risk factor, Stroke, business.industry, Mortality rate, Cognitive disorder, Middle Aged, medicine.disease, Multivariate Analysis, Cohort, Physical therapy, Neurology (clinical), business
Abstract

Causes of early and delayed death after stroke differ. It has been suggested that delayed mortality rate was increased in patients with post-stroke dementia. Prestroke dementia is frequent: its influence on survival in stroke patients has never been evaluated. The aim of this study was to evaluate the influence of prestroke dementia on early and delayed mortality rate after stroke. In a cohort of 202 consecutive stroke patients agedor= 40 years admitted between November 1995 and May 1996 in a primary care center, the prevalence of prestroke dementia was determined using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) with a cut-off of 104. Patients were followed-up for 3 years. Statistics were performed using life-table methods. Of 202 patients, 33 had prestroke dementia. Of 142 survivors at month-6, 44 were demented, of them 15 having prestroke and 29 new-onset post-stroke dementia. No patient was lost to follow-up. The risk of death at month-6 was higher in patients with prestroke dementia (RR 2.7; 95 % CI: 1.6-4.8). However, independent predictors of early death were age, severity of the deficit at admission, type and etiology of stroke. The risk of delayed death was higher in patients with prestroke dementia (RR 4.97; 95 % CI: 1.76-13.98) as in patients with new-onset post-stroke dementia (RR 6.24; 95 % CI: 2.67-14.57), compared with non-demented patients. The mortality rate did not differ between patients with prestroke and new-onset post-stroke dementia. Dementia at month-6 was an independent predictor of delayed death (RR 5.7; 95 % CI: 2.4-13.4), with age and stroke recurrence. Causes of death did not differ between demented and non-demented patients. Dementia adversely influences vital outcome in stroke patients, perhaps partly because the therapeutic approach differs between demented and non-demented patients.

Published
2003
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32. DAPHNE: A New Tool for the Assessment of the Behavioral Variant of Frontotemporal Dementia

Author

Christelle Evrard, Samuel Bulteau, Claire Boutoleau-Bretonnière, Catherine Thomas-Antérion, Frédérique Etcharry-Bouyx, Martine Vercelletto, Laëtitia Rocher, Tiphaine Charriau, Aurélie Richard-Mornas, Florence Lebert, Florence Pasquier, Sophie Auriacombe, Jean-Benoit Hardouin, Anne Sauvaget, Cédric Bretonnière, Pascal Derkinderen, MethodS in Patients-centered outcomes and HEalth ResEarch (SPHERE), Université de Tours-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR des Sciences Pharmaceutiques et Biologiques, Université de Nantes (UN)-Université de Nantes (UN), Service de Neurologie [Lille], Hôpital Roger Salengro [Lille]-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Université de Tours (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR des Sciences Pharmaceutiques et Biologiques, Département de neurologie [Lille], and Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)

Subjects
medicine.medical_specialty, Bipolar disorder, Cognitive Neuroscience, Perseveration, media_common.quotation_subject, [SDV]Life Sciences [q-bio], Validity, lcsh:Geriatrics, lcsh:RC346-429, Alzheimer’s disease, Progressive supranuclear palsy, Neglect, External validity, medicine, Apathy, Original Research Article, Psychiatry, lcsh:Neurology. Diseases of the nervous system, ComputingMilieux_MISCELLANEOUS, media_common, Alzheimer's disease, medicine.disease, Scale, Behavioral disorders, lcsh:RC952-954.6, Psychiatry and Mental health, medicine.symptom, Psychology, Frontotemporal dementia, Clinical psychology
Abstract

Background: The diagnosis of behavioral variant of frontotemporal dementia (bvFTD) relies primarily on clinical features and remains challenging. The specificity of the recently revised criteria can be disappointing, justifying development of new clinical tools. Objective: We produced a behavioral inventory named DAPHNE. This scale (adapted from Rascovsky's criteria) explores six domains: disinhibition, apathy, perseverations, hyperorality, personal neglect and loss of empathy. It is composed of ten items (five answer categories). The aim was (1) to assess the validity and reliability of DAPHNE and (2) to evaluate its contribution in differentiating patients. Methods: Two scores were computed: DAPHNE-6 (screening) from the six domains and DAPHNE-40 (diagnosis) from the ten items. Reliability and reproducibility were assessed. External validity was studied with the Frontal Behavioral Inventory (FBI) and the Frontotemporal Behavioral Scale (FBS). Finally, the diagnostic performance of DAPHNE was compared to revised criteria, FBI and FBS. Results: DAPHNE was administered to the caregivers of 89 patients, 36 with bvFTD, 22 with Alzheimer's disease, 15 with progressive supranuclear palsy and 16 with bipolar disorder. Reliability and reproducibility were excellent, as was external validity. DAPHNE-6 allowed bvFTD diagnosis (score ≥4) with a sensitivity of 92%, while DAPHNE-40 (score ≥15) had a specificity of 92%. Conclusion: We demonstrate excellent psychometric features for DAPHNE. This quick tool could help for both diagnosing and screening bvFTD.

Published
2015
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33. Tau aggregation in the hippocampal formation: an ageing or a pathological process?

Author

Jean-Philippe David, André Delacourte, Florence Lebert, Nicolas Sergeant, Claude-Alain Maurage, A. Wattez, and Florence Pasquier

Subjects
Amyloid, Aging, tau Proteins, Disease, Hippocampal formation, Hippocampus, Biochemistry, Mice, Endocrinology, Alzheimer Disease, Genetics, medicine, Animals, Humans, Cognitive impairment, Molecular Biology, Pathological, Process (anatomy), Aged, business.industry, Multidisciplinary analysis, Brain, Cell Biology, medicine.disease, Tauopathies, Ageing, Nerve Degeneration, Tauopathy, business, Neuroscience
Abstract

Tauopathy is a concept to describe different genetic or metabolic dysfunctions of tau proteins that generate most of the known dementing disorders. Tauopathy is a degenerating process that also affects the entorhinal formation, and then the hippocampal formation in ageing. In Alzheimer's disease (AD), a disease due to APP dysfunction, a similar tauopathy process in observed in neocortical areas, well correlated to cognitive impairment. One important gap of knowledge is the relationship between tauopathy in the hippocampal formation, ageing, AD, and cognitive impairment. Here we show that the multidisciplinary analysis of numerous brains from non-demented and demented patients suggests the following observations: tauopathy of the hippocampal formation in humans is age-related but not an age-dependent process, also independent of AD, but amplified by APP dysfunctions. Tauopathy in the entorhinal and hippocampal formation could be another type of pathological dysfunction of tau proteins, and a therapeutic target to delay AD. Relevant animal models are desperately needed to address this issue.

Published
2002
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34. Nonoverlapping but synergetic tau and APP pathologies in sporadic Alzheimer's disease

Author

Nicolas Sergeant, André Delacourte, Jean-Philippe David, Florence Lebert, Florence Pasquier, Claude-Alain Maurage, Danie Champain, and A. Wattez

Subjects
Pathology, medicine.medical_specialty, Amyloid, Tau protein, tau Proteins, Amyloid beta-Protein Precursor, Mice, Mice, Neurologic Mutants, Degenerative disease, Alzheimer Disease, medicine, Amyloid precursor protein, Animals, Humans, Prospective Studies, Brain Chemistry, Amyloid beta-Peptides, biology, Chemistry, Neurodegeneration, Neurotoxicity, Brain, Amyloidosis, Human brain, medicine.disease, Peptide Fragments, medicine.anatomical_structure, Solubility, biology.protein, Neurology (clinical), Alzheimer's disease, Neuroscience
Abstract

Objective: To determine the spatiotemporal mapping of tau pathologies and insoluble pools of Aβ in aging and sporadic AD, and their contribution to the physiopathologic, clinical, and neuropathologic features. Methods: The authors studied 130 patients of various ages and different cognitive status, from nondemented controls (n = 60) to patients with severe definite AD (n = 70) who were followed prospectively. Insoluble Aβ 42 and 40 species were fully solubilized and quantified in the main neocortical areas, with a new procedure adapted to human brain tissue. Tau pathology staging was determined in 10 different brain areas, using Western blots. Results: In AD, there is a constellation of amyloid phenotypes, extending from cases with exclusively aggregated Aβ 42 to cases with, in addition, large quantities of insoluble Aβ 40 species. Five other points were observed: 1) There was no spatial and temporal overlap in the distribution of these two insoluble Aβ species in cortical brain areas. 2) In contrast to solubilized Aβ 40 aggregates composed essentially of monomers and dimers, solubilized Aβ 42 was essentially observed as dimers and multimers. 3) Aβ 42 aggregates were observed at the early stages of tau pathology, whereas the insoluble Aβ 40 pool was found at the last stages. 4) During the progression of the disease, Aβ aggregates increase in quantity and heterogeneity, in close parallel to the extension of tau pathology. 5) There was no spatial overlap between Aβ aggregation that is widespread and heterogeneously distributed in cortical areas and tau pathology that is progressing sequentially, stereotypically, and hierarchically. Conclusions: These observations demonstrate that Aβ 42 aggregation, and not Aβ 40, is the marker that is close to Alzheimer etiology. It should be the main target for the early biological diagnosis of AD and modeling. Furthermore, the spatial mismatch between amyloid s-precursor protein (APP) and tau pathologies in cortical brain areas demonstrates that neurodegeneration is not a direct consequence of extracellular Aβ neurotoxicity. Hence, there is a synergetic effect of APP dysfunction, revealed by Aβ aggregation, on the neuron-to-neuron propagation of tau pathology.

Published
2002
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35. Poststroke dementia: Incidence and relationship to prestroke cognitive decline

Author

D. Guerouaou, Hilde Hénon, Didier Leys, I. Durieu, Florence Lebert, and Florence Pasquier

Subjects
Adult, Male, medicine.medical_specialty, Pediatrics, Disease-Free Survival, Brain Ischemia, Age Distribution, Risk Factors, Informant Questionnaire on Cognitive Decline in the Elderly, mental disorders, medicine, Humans, Dementia, Cognitive decline, Risk factor, Vascular dementia, Stroke, Cerebral Hemorrhage, Dementia, Vascular, Incidence, Cognitive disorder, Leukoaraiosis, medicine.disease, Surgery, Multivariate Analysis, Female, Neurology (clinical), Cognition Disorders, Psychology
Abstract

Objective: To evaluate the 3-year incidence of poststroke dementia (PSD) and the influence of prestroke cognitive decline. Methods: The authors evaluated prestroke cognitive functions in 202 consecutive stroke patients ≥40 years old using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE), with a cut-off of 104 for the diagnosis of dementia. Six months and then annually after stroke, dementia was reassessed. The diagnosis of dementia was based on the International Classification of Diseases, 10th revision criteria in survivors who underwent a visit with a neurologist, or on the IQCODE score obtained by telephone contact with the family in survivors who did not. Statistics were performed using life-table methods. Results: Thirty-three patients were excluded because of prestroke dementia. In the 169 remaining patients, the cumulative proportion of patients with dementia was 28.5% at the end of the follow-up period, with most of PSD occurring during the first 6 months. Using multivariate analysis, independent predictors of PSD were aging, preexisting cognitive decline, severity of deficit at admission, diabetes mellitus, and silent infarcts. Leukoaraiosis was an independent predictor of PSD when prestroke cognitive decline was not taken into account. The presumed etiology of dementia was vascular dementia (VaD) in two-thirds of patients and AD in one-third. Conclusions: The risk of PSD is high, and increased in patients with prestroke cognitive decline, with about one-third of patients meeting the criteria for AD and two-thirds meeting the criteria for VaD. These results confirm that, in stroke patients, an underlying degenerative pathology may play a role in the development of PSD.

Published
2001
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36. Frontotemporal Behavioral Scale

Author

Lydie Souliez, Henri Petit, Florence Pasquier, and Florence Lebert

Subjects
Male, Pediatrics, medicine.medical_specialty, Neuropsychological Tests, Temporal lobe, Diagnosis, Differential, Central nervous system disease, Degenerative disease, Alzheimer Disease, mental disorders, medicine, Humans, Dementia, Vascular dementia, Internal-External Control, Aged, Aged, 80 and over, Psychiatric Status Rating Scales, Dementia, Vascular, nutritional and metabolic diseases, Middle Aged, medicine.disease, Temporal Lobe, Frontal Lobe, nervous system diseases, Psychiatry and Mental health, Clinical Psychology, Frontal lobe, Geriatrics and Gerontology, Alzheimer's disease, Mental Status Schedule, Psychology, Gerontology, Neuroscience, Frontotemporal dementia
Abstract

At autopsy, frontotemporal dementia (FTD) account for up to 20% of degenerative dementia cases, although FTDs are underrecognized in memory clinics. FTDs are confused with Alzheimer disease (AD) or vascular dementia (VaD). These misdiagnosis may affect the results of AD pharmacological trials. The first manifestations of FTD are behavioral abnormalities. The aim of this study was to assess a behavioral scale of frontal lobe dysfunction and to determine a behavioral cutoff to diagnose early FTD and distinguish it from AD and VaD. The score of the behavioral frontotemporal lobe dysfunction assessment scale was higher in FTD than in other dementias (p < 0.0001). With a cutoff of 3 points on the scale, FTD patients were diagnosed with a specificity of 95% and sensitivity of 91%. Noncognitive symptoms known to be institutionalization factors could contribute to differences between etiologies of mild dementia.

Published
1998
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37. Tacrine efficacy in Lewy body dementia

Author

Florence Lebert, Lydie Souliez, Florence Pasquier, and Henri Petit

Subjects
Male, medicine.medical_specialty, medicine.medical_treatment, Central nervous system disease, Cognition, Degenerative disease, Alzheimer Disease, Internal medicine, medicine, Memory span, Humans, Dementia, Aged, Cholinesterase, Aged, 80 and over, Chemotherapy, biology, Lewy body, medicine.disease, Surgery, Psychiatry and Mental health, Treatment Outcome, Tacrine, biology.protein, Female, Lewy Bodies, Cholinesterase Inhibitors, Geriatrics and Gerontology, Psychology, hormones, hormone substitutes, and hormone antagonists, medicine.drug
Abstract

Background. Response to tacrine varies among patients with Alzheimer's disease (AD). Lewy body dementia (LBD) could be a high responder subtype of AD. The aim of the study was to compare the effects of tacrine in LBD and AD. Methods. Seventy-five consecutive outpatients with mild or moderate AD were screened. Tacrine was given at a dose of 40 mg/day during 6 weeks. During the next 6 weeks, the patients were treated with 80 mg/day and afterwards with 120 mg/day. Patients were assessed at baseline and treated with a dose of 120 mg/day tacrine for 2 weeks. Results. Analysis was performed on 39 patients (AD, N = 20; LBD, N = 19). Eight patients were lost to follow-up, eight patients manifested with side-effects, six suffered from an intercurrent somatic disease during the study and 14 patients had poor compliance or were treated with incompatible drugs. Twenty-two patients (11 AD/11 LBD) increased their cognitive performances with tacrine. Among the 22 patients, the improvement differed between the AD and the LBD groups. In AD, conceptualization improved; in LBD, the improvements occurred in verbal initiation and digit span. Conclusion. This study emphasizes the importance of using appropriate tests to determine the positive effects of pharmacological treatments.

Published
1998
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38. Explicit Memory in Frontotemporal Dementia: The Role of Medial Temporal Atrophy

Author

Florence Pasquier, Jean-Pierre Pruvo, Florence Lebert, I. Lavenu, and Henri Petit

Subjects
Male, Cognitive Neuroscience, Hippocampus, Temporal lobe, Memory, mental disorders, medicine, Explicit memory, Humans, Dementia, Memory impairment, Aged, Memory clinic, Middle Aged, medicine.disease, Temporal Lobe, Frontal Lobe, Psychiatry and Mental health, Mental Recall, Female, Pick's disease, Atrophy, Geriatrics and Gerontology, Tomography, X-Ray Computed, Psychology, Neuroscience, Frontotemporal dementia
Abstract

In our memory clinic experience, memory impairment differs widely in patients with frontotemporal dementia (FTD). We searched for a correlation between explicit memory disturbance assessed with the Grober and Buschke test and medial temporal atrophy on CT scan in 22 consecutive patients with FTD. Five of the 22 patients had a medial temporal lobe (MTL) atrophy. There was no significant difference between the two groups for the demographic characteristics. Free recall, cued recall and the learning curve were significantly better in patients without MTL atrophy. The patients with MTL atrophy made more intrusions. We found a positive correlation between total recall and cued recall and the mean of medial temporal lobe measurement. These results are in agreement with the role of the hippocampal formation in the memory process. In our group, the ratio of patients with MTL atrophy is similar to the ratio of Pick’s disease in frontotemporal dementia. In histological series more severe hippocampal atrophy are reported in Pick’s disease. Therefore MTL atrophy on CT scan could be a marker of Pick’s disease in FTD.

Published
1998
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39. Frontotemporal dementia and its subtypes: A genome-wide association study

Author

Yolande A.L. Pijnenburg, Wei Gu, Harro Seelaar, Robert Perneczky, Alfredo Postiglione, Ronald C. Petersen, Timothy D. Griffiths, Pau Pastor, Marc Cruts, Elise G.P. Dopper, Sabrina Pichler, Chiara Fenoglio, Patrizia Rizzu, Adeline Rollin, Maria Serpente, Peter Heutink, Sandro Sorbi, Lauren Bartley, Maria Landqvist Waldö, Luigi Ferrucci, William S. Brooks, Luisa Benussi, William W. Seeley, Maria Anfossi, Atik Baborie, Innocenzo Rainero, Rosa Capozzo, Alessandro Padovani, Stefano F. Cappa, Glenda M. Halliday, Jørgen E. Nielsen, Sara Ortega-Cubero, Vivianna M. Van Deerlin, Ekaterina Rogaeva, Mike A. Nalls, Giacomina Rossi, Alberto Lleó, Edward D. Huey, Jordi Clarimón, Simon Mead, Janine Diehl-Schmid, John Q. Trojanowski, Adaikalavan Ramasamy, Matthias Riemenschneider, John Hardy, Annibale Alessandro Puca, Cristina Razquin, Mercè Boada, Martine Vercelletto, Isabelle Le Ber, Graziella Milan, Johannes Attems, Francesca Frangipane, Jason D. Warren, Lena E. Hjermind, John R. Hodges, Gianluigi Forloni, Dennis W. Dickson, Daniela Galimberti, Elisa Rubino, Karin Nilsson, Raffaele Maletta, Christine Van Broeckhoven, Valeria Novelli, Anna Richardson, Anna Karydas, David S. Knopman, Nick C. Fox, Stuart Pickering-Brown, Carlos Cruchaga, Isabel Hernández, Livia Bernardi, Philip Scheltens, Martin N. Rossor, Julie S. Snowden, Massimo Franceschi, Rosa Rademakers, Bruce L. Miller, Alan J. Thomas, Florence Lebert, Matthew C. Baker, Jonathan D. Rohrer, Keith A. Josephs, Tim Van Langenhove, Fabrizio Tagliavini, Carol Dobson-Stone, Elizabeth Thompson, Silvia Bagnoli, Barbara Borroni, Sara Rollinson, Irene Piaceri, David M. A. Mann, Bernd Ibach, Ian G. McKeith, Agustín Ruiz, Huw R. Morris, Giancarlo Logroscino, Maura Gallo, Elena Alonso, Alexis Brice, Adrian Danek, Paolo Sorrentino, Nicoletta Smirne, Raffaele Ferrari, Panagiotis Alexopoulos, Johannes C. M. Schlachetzki, Alexander Gerhard, Manuel Mayhaus, Alexander Kurz, Amalia C. Bruni, Michael Tierney, Didier Hannequin, William Deschamps, Florence Pasquier, Joseph E. Parisi, Rafael Blesa, Elio Scarpini, Ian R. A. Mackenzie, Peter R. Schofield, Giuliano Binetti, Evelyn Jaros, Julie van der Zee, John Collinge, Maria Elena Conidi, Howard J. Rosen, Caroline Graff, Christer Nilsson, Huei-Hsin Chiang, Nigel J. Cairns, Jordan Grafman, Eric M. Wassermann, Parastoo Momeni, Maria Grazia Spillantini, Ging-Yuek Robin Hsiung, Andrew B. Singleton, Chiara Cupidi, James Uphill, Dimitrios Kapogiannis, Bradley F. Boeve, Christopher Morris, Vincent Deramecourt, Giorgio Giaccone, James B. Rowe, Murray Grossman, Benedetta Nacmias, Roberta Ghidoni, Véronique Golfier, Dena G. Hernandez, Lorenzo Pinessi, Neill R. Graff-Radford, John C. van Swieten, Pietro Pietrini, Gilles Gasparoni, Peter St George-Hyslop, Mark Kristiansen, Eric Haan, Olivier Piguet, John B.J. Kwok, Human genetics, Neurology, NCA - neurodegeneration, Surgery, Clinical Genetics, Erasmus MC other, Ferrari, R, Hernandez, Dg, Nalls, Ma, Rohrer, Jd, Ramasamy, A, Kwok, Jb, Dobson Stone, C, Brooks, W, Schofield, Pr, Halliday, Gm, Hodges, Jr, Piguet, O, Bartley, L, Thompson, E, Haan, E, Hern?ndez, I, Ruiz, A, Boada, M, Borroni, B, Padovani, A, Cruchaga, C, Cairns, Nj, Benussi, L, Binetti, G, Ghidoni, R, Forloni, G, Galimberti, D, Fenoglio, C, Serpente, M, Scarpini, E, Clarim?n, J, Lle?, A, Blesa, R, Wald?, Ml, Nilsson, K, Nilsson, C, Mackenzie, Ir, Hsiung, Gy, Mann, Dm, Grafman, J, Morris, Cm, Attems, J, Griffiths, Td, Mckeith, Ig, Thomas, Aj, Pietrini, P, Huey, Ed, Wassermann, Em, Baborie, A, Jaros, E, Tierney, Mc, Pastor, P, Razquin, C, Ortega Cubero, S, Alonso, E, Perneczky, R, Diehl Schmid, J, Alexopoulos, P, Kurz, A, Rainero, I, Rubino, E, Pinessi, L, Rogaeva, E, St George Hyslop, P, Rossi, G, Tagliavini, F, Giaccone, G, Rowe, Jb, Schlachetzki, Jc, Uphill, J, Collinge, J, Mead, S, Danek, A, Van Deerlin, Vm, Grossman, M, Trojanowski, Jq, van der Zee, J, Deschamps, W, Van Langenhove, T, Cruts, M, Van Broeckhoven, C, Cappa, Sf, Le Ber, I, Hannequin, D, Golfier, V, Vercelletto, M, Brice, A, Nacmias, B, Sorbi, S, Bagnoli, S, Piaceri, I, Nielsen, Je, Hjermind, Le, Riemenschneider, M, Mayhaus, M, Ibach, B, Gasparoni, G, Pichler, S, Gu, W, Rossor, Mn, Fox, Nc, Warren, Jd, Spillantini, Mg, Morris, Hr, Rizzu, P, Heutink, P, Snowden, J, Rollinson, S, Richardson, A, Gerhard, A, Bruni, Ac, Maletta, R, Frangipane, F, Cupidi, C, Bernardi, L, Anfossi, M, Gallo, M, Conidi, Me, Smirne, N, Rademakers, R, Baker, M, Dickson, Dw, Graff Radford, Nr, Petersen, Rc, Knopman, D, Josephs, Ka, Boeve, Bf, Parisi, Je, Seeley, Ww, Miller, Bl, Karydas, Am, Rosen, H, van Swieten, Jc, Dopper, Eg, Seelaar, H, Pijnenburg, Ya, Scheltens, P, Logroscino, G, Capozzo, R, Novelli, V, Puca, Aa, Franceschi, M, Postiglione, Alfredo, Milan, G, Sorrentino, P, Kristiansen, M, Chiang, Hh, Graff, C, Pasquier, F, Rollin, A, Deramecourt, V, Lebert, F, Kapogiannis, D, Ferrucci, L, Pickering Brown, S, Singleton, Ab, Hardy, J, and Momeni, P.

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Genotype, Semantic dementia, Genome-wide association study, Locus (genetics), classification [Frontotemporal Dementia], methods [Genome-Wide Association Study], diagnosis [Frontotemporal Dementia], C9orf72, mental disorders, medicine, Dementia, Humans, ddc:610, genetics [Frontotemporal Dementia], Aged, Genetics, Aged, 80 and over, Genetic heterogeneity, Middle Aged, medicine.disease, Frontotemporal Dementia, Female, Human medicine, Neurology (clinical), Alzheimer's disease, Psychology, Frontotemporal dementia, Genome-Wide Association Study
Abstract

Summary Background Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. Mutations in three genes— MAPT , GRN , and C9orf72 —have been associated with FTD. We sought to identify novel genetic risk loci associated with the disorder. Methods We did a two-stage genome-wide association study on clinical FTD, analysing samples from 3526 patients with FTD and 9402 healthy controls. To reduce genetic heterogeneity, all participants were of European ancestry. In the discovery phase (samples from 2154 patients with FTD and 4308 controls), we did separate association analyses for each FTD subtype (behavioural variant FTD, semantic dementia, progressive non-fluent aphasia, and FTD overlapping with motor neuron disease [FTD-MND]), followed by a meta-analysis of the entire dataset. We carried forward replication of the novel suggestive loci in an independent sample series (samples from 1372 patients and 5094 controls) and then did joint phase and brain expression and methylation quantitative trait loci analyses for the associated (p −8 ) single-nucleotide polymorphisms. Findings We identified novel associations exceeding the genome-wide significance threshold (p −8 ). Combined (joint) analyses of discovery and replication phases showed genome-wide significant association at 6p21.3, HLA locus (immune system), for rs9268877 (p=1·05 × 10 −8 ; odds ratio=1·204 [95% CI 1·11–1·30]), rs9268856 (p=5·51 × 10 −9 ; 0·809 [0·76–0·86]) and rs1980493 (p value=1·57 × 10 −8 , 0·775 [0·69–0·86]) in the entire cohort. We also identified a potential novel locus at 11q14, encompassing RAB38 / CTSC (the transcripts of which are related to lysosomal biology), for the behavioural FTD subtype for which joint analyses showed suggestive association for rs302668 (p=2·44 × 10 −7 ; 0·814 [0·71–0·92]). Analysis of expression and methylation quantitative trait loci data suggested that these loci might affect expression and methylation in cis . Interpretation Our findings suggest that immune system processes (link to 6p21.3) and possibly lysosomal and autophagy pathways (link to 11q14) are potentially involved in FTD. Our findings need to be replicated to better define the association of the newly identified loci with disease and to shed light on the pathomechanisms contributing to FTD. Funding The National Institute of Neurological Disorders and Stroke and National Institute on Aging, the Wellcome/MRC Centre on Parkinson's disease, Alzheimer's Research UK, and Texas Tech University Health Sciences Center.

Published
2014
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40. Frontotemporal dementia

Author

Vincent Deramecourt, Florence Lebert, and Florence Pasquier

Subjects
mental disorders, nutritional and metabolic diseases, nervous system diseases, 3. Good health
Abstract

Frontotemporal dementia (FTD) is the second most common form of dementia in persons younger than 65 years after Alzheimer’s disease. The FTD spectrum is characterized by clinical, molecular and genetic heterogeneity. Core features of FTD are behavioural and language manifestations and the clinical spectrum of FTD currently includes a behavioural variant, progressive nonfluent aphasia and semantic dementia. The most common behavioural features are disinhibition, apathy, loss of empathy, hyperorality and perseveration. Neuroimaging usually demonstrates focal atrophy and hypometabolism in the anterior part of the frontal and temporal lobes. A careful history and neuropsychological examination, and judicious use of neuroimaging, can help distinguish FTD from other common forms of dementia, especially Alzheimer’s disease, vascular dementia, and dementia with Lewy bodies. Although no specific pharmacological treatments for FTD exists, symptom management with serotonin reuptake inhibitors and non pharmacological interventions have been shown to be beneficial.

Published
2013
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41. P2–221: Frontotemporal lobar degeneration: Any link between tau and TDP‐43?

Author

Nicolas Sergeant, Dominique Campion, Anthony Papegaey, Vincent Deramecourt, Luc Buée, Valérie Buée-Scherrer, Magalie Lecourtois, Florence Pasquier, and Florence Lebert

Subjects
Pathology, medicine.medical_specialty, Epidemiology, business.industry, Health Policy, Frontotemporal lobar degeneration, medicine.disease, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Medicine, Neurology (clinical), Geriatrics and Gerontology, business, Link (knot theory)
Published
2013
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42. Generation Effect in Short-Term Verbal and Visuospatial Memory: Comparisons Between Dementia of Alzheimer Type and Dementia of Frontal Lobe Type

Author

Florence Lebert, Florence Pasquier, Henri Petite, Pierre Leconte, and Lydie Souliez

Subjects
Male, inorganic chemicals, medicine.medical_specialty, Cognitive Neuroscience, Experimental and Cognitive Psychology, Audiology, Spatial memory, Alzheimer Disease, mental disorders, medicine, Humans, Dementia, In patient, Aged, Tomography, Emission-Computed, Single-Photon, Verbal Learning, medicine.disease, Frontal Lobe, Cerebrovascular Disorders, Memory, Short-Term, Neuropsychology and Physiological Psychology, Frontal lobe, Space Perception, Early dementia, Visual Perception, Female, Verbal memory, Alzheimer's disease, Tomography, X-Ray Computed, Psychology, Generation effect, Cognitive psychology
Abstract

Memory deficit is the predominant presenting symptom in dementia. To compare short-term memory (STM) deficit in early dementia of Alzheimer type (DAT) vs frontal lobe type (DFT), and determine the residual memory capacity for stimulation, the generation effect (the memory advantage of items generated rather than read) was tested on verbal and visuospatial STM in patients with DAT (n = 10), DFT (n = 9) and in age-matched normal controls (n = 12). The generation effect enhanced performance in all groups. However, the profile of STM deficit differed in the two dementias: verbal and visuospatial memory were both decreased in DAT vs verbal memory only in DFT. These results provide a further criterion for differentiating between DAT and DFT, and show that memory performance can be enhanced in early dementia using techniques such as the generation effect.

Published
1996
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43. Sundowning syndrome in demented patients without neuroleptic therapy

Author

Henri Petit, Florence Lebert, and Florence Pasquier

Subjects
Aging, medicine.medical_specialty, Pediatrics, Sleep disorder, education.field_of_study, Health (social science), Evening, Exacerbation, Sundowning, Population, medicine.disease, Arousal, Delusion, medicine, Dementia, Geriatrics and Gerontology, medicine.symptom, Psychiatry, Psychology, education, Gerontology
Abstract

Characterisation of sundowning syndrome, defined as 'an exacerbation of symptoms indicating increased arousal or impairment in late afternoon, evening or at night, among elderly demented individuals', is complicated by neuroleptic therapy and frequent failure to specify the nature of the associated dementia. Screening by a memory disorders unit of an institutionalized population of 30 neuroleptic-free demented patients revealed 8 sundowners, with diagnoses of probable Alzheimer's disease (n = 5), frontal lobe dementia (n = 1), Lewy body disease (n = 1), and sequelae of herpes encephalitis (n = 1). Sundowners did not differ from non-sundowners in age, Mini Mental State score, degree of temporal and spatial disorientation or perceptual delusion. Sundowning was related to restlessness (P < 0.0001), sleep disorder (P < 0.003) and a history of hypotension lipothymia (P < 0.08). These results provide further evidence for a chronobiological explanation of sundowning syndrome.

Published
1996
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44. Contents Vol. 17, 2004

Author

Glenda M. Halliday, Martin Sjöbeck, Eileen H. Bigio, Peter Heutink, Jennifer L. Whitwell, Ronald Kim, Norbert Schuff, Yolande A.L. Pijnenburg, A.G. Jones, Richard J. Perry, Chris DeVita, Katherine P. Rankin, Sonia M. Rosso, Lars Lannfelt, Christina Elfgren, Susanne Gydesen, Yoshifumi Koshino, David G. Munoz, Karin Nilsson, Corey T. McMillan, Susanne Froelich Fabre, Elizabeth M. C. Fisher, M. Wittmann, Sara Brockstedt, Elna-Marie Larsson, Anders Gade, Masaaki Iijima, Anne M. Lipton, Bernd Ibach, Ian R. A. Mackenzie, Martin N. Rossor, Bruce L. Miller, VM Anderson, Carl W. Cotman, Jerry Brown, A Brun, Howard Feldman, Thomas S. Harris, Jillian J. Kril, Manabu Ikeda, Jimmy Lätt, Tomokazu Kidani, Jovanka Ostojic, Kari Dennis, Julene K. Johnson, Katherine Pace-Savitsky, S. Poljansky, Wouter Kamphorst, Joel H. Kramer, Murray Grossman, Florence Pasquier, Harald Hampel, Kaoru Sugimori, Andrew Kertesz, Catherine Lomen-Hoerth, James C. Gee, Freek Gillissen, M. Koller, Lisa Chakrabarti, Guido F. Schauer, Ingmar Rosén, G. Hajak, Florence Richard, Hirotaka Tanabe, John Collinge, Christine Hasenbroekx, L. Gustafson, Katsuji Kobayashi, Nick C. Fox, Stuart Pickering-Brown, Philip Scheltens, Frederick J. Bonte, Tove Thusgaard, Rachael I. Scahill, Masao Shimazaki, Linda S. Hynan, Keith A. Josephs, Shigetoshi Kuroda, Florence Lebert, Despina Yancopoulou, Ulla Passant, Stefan J. Teipel, Hiroshi Ujike, Asger Sorensen, Elizabeth Head, Peter Johannsen, Gaia Skibinski, Robert W. Levenson, Arne Brun, Howard J. Rosen, W. Barta, Helen-Ann Comstock, Masahiro Hayashi, Lars Gustafson, Cees Jonker, Dennis W. Dickson, Rivka Ravid, Peachie Moore, Charles L. White, Brent A. Vogt, Magnus Sjögren, Esther van Herpen, Maria Grazia Spillantini, Michael W. Weiner, Willy Stekke, Takeshi Ishihara, Raul Benavides, Tomohisa Ishikawa, Elisabet Englund, John C. van Swieten, and Hiroyuki Nakano

Subjects
Psychiatry and Mental health, Cognitive Neuroscience, Geriatrics and Gerontology
Published
2004
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45. [From Pick's disease to frontotemporal dementia]

Author

Florence, Pasquier, Vincent, Deramecourt, and Florence, Lebert

Subjects
Diagnosis, Differential, Pick Disease of the Brain, Frontotemporal Dementia, Humans, Behavioral Symptoms
Abstract

Frontotemporal dementias (FTD) are defined by a gradual change in social conduct, behavior and language, associated with frontal and anterior temporal lobe degeneration. The clinicalfeatures depend on the location of the degenerative process. In the last 20 years, increasingly specific and sensitive operational criteria have been established. Ongoing neuropathological and genetic studies have highlighted overlaps between FTD, motor neuron disease, and atypical parkinsonian syndromes (supranuclear palsy, corticobasal degeneration). They have also provided a better knowledge of the pathophysiology of FTD, and new specific therapeutic targets. These dementias, which usually occur before the age of 65 years, are now better recognized but are still underdiagnosed and often initially mistaken for psychiatric illnesses. Healthcare professionals managing these patients must therefore be better informed Serotonergic agents provide a symptomatic improvement, but environmental adaptation, prevention of language and swallowing difficulties, and information and support for the family and caregivers remain essential.

Published
2013

46. Verbal fluency in dementia of frontal lobe type and dementia of Alzheimer type

Author

L. Grymonprez, Florence Pasquier, Henri Petit, and Florence Lebert

Subjects
Male, medicine.medical_specialty, Neuropsychological Tests, Audiology, behavioral disciplines and activities, Developmental psychology, Central nervous system disease, Fluency, Alzheimer Disease, Parietal Lobe, mental disorders, medicine, Humans, Dementia, Verbal fluency test, Aged, Tomography, Emission-Computed, Single-Photon, Language Disorders, medicine.diagnostic_test, Verbal Behavior, Parietal lobe, Neuropsychological test, Middle Aged, medicine.disease, Frontal Lobe, Psychiatry and Mental health, Frontal lobe, Cerebrovascular Circulation, Female, Surgery, Neurology (clinical), Alzheimer's disease, Psychology, Research Article
Abstract

This study compares semantic (category) and letter-initial verbal fluency performance in dementia of frontal lobe type, dementia of Alzheimer type, and control subjects matched for age, sex, and level of education. As well as demographic characteristics, patients were matched for severity of dementia as estimated by the mini mental scale (23.2 (SD 4.9)). All patients with dementia of frontal lobe type had a frontal hypoperfusion on single photon emission computed tomography whereas patients with dementia of Alzheimer type showed mainly posterior deficits. Patients had significantly lower verbal fluency than controls but those with dementia of frontal lobe type did not differ from those with dementia of Alzheimer type in the number of words generated, intrusions, or preservations. Category fluency was more impaired than letter fluency in both dementias. No correlation between frontal index, frontal/parietal index, and fluency was found. Verbal fluency tests are sensitive tools for detecting dementia but do not seem useful in distinguishing between patients with dementia of Alzheimer type and those with dementia of frontal lobe type in early disease.

Published
1995
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47. Clinical, neuropathological, and biochemical characterization of the novel tau mutation P332S

Author

Simon Dujardin, Nicolas Sergeant, Fabienne Clot, Claude-Alain Maurage, Valérie Buée-Scherrer, Florence Lebert, Isabelle Le Ber, Alexis Brice, Morvane Colin, Francisco-Jose Fernandez-Gomez, Luc Buée, Vincent Deramecourt, and Florence Pasquier

Subjects
Proband, Male, Pathology, medicine.medical_specialty, tau Proteins, Biology, Exon, Atrophy, Genetic variation, medicine, Humans, Pathological, Anarthria, Genetics, Aged, 80 and over, General Neuroscience, Genetic Variation, General Medicine, Frontotemporal lobar degeneration, Middle Aged, medicine.disease, biology.organism_classification, Phenotype, Pedigree, Psychiatry and Mental health, Clinical Psychology, HEK293 Cells, Mutation, Female, Geriatrics and Gerontology, Frontotemporal Lobar Degeneration, Follow-Up Studies
Abstract

MAPT mutations cause autosomal dominant frontotemporal lobar degeneration. These diseases are characterized by considerable heterogeneity in their clinical, neuropathological, and biochemical presentations. We describe the full character- ization of a family with autosomal dominant frontotemporal lobar degeneration caused by a novel MAPT mutation. Clinical, imaging, neuropathological, and biochemical data are presented. The proband was a woman who died at 85 years old, 25 years after the onset of a slowly progressive and isolated anarthria and opercular syndrome. The pathological examination of her brain showed marked atrophy of primary motor and premotor cortices, associated with predominant neuronal tau-positive lesions mimicking Pick bodies. At the biochemical level, the six tau isoforms aggregate to display a pathological triplet at 60, 64, and 69 kDa. Two of her sons presented at 48 and 50 years old with a right temporal variant of frontotemporal degeneration char- acterized by severe prosopagnosia, semantic impairment, and behavioral modifications. In these three patients, the molecular analysis of MAPT showed the c.1945C>T mutation on exon 11 resulting in the P332S substitution in tau sequence. This mutation changes the PGGG motif of the third repeat domain of the protein and therefore reduces the ability of tau to bind microtubules. From a clinical point of view, this mutation is associated with considerable intrafamilial phenotypic variation.

Published
2012

48. [Alzheimer's disease and related disorders: specificity of young onset patients, including ethical aspects]

Author

Pierre Boitte, Florence Lebert, Armelle de Bouvet, and Florence Pasquier

Subjects
Gerontology, Lewy Body Disease, Male, medicine.medical_specialty, Yod, National Health Programs, media_common.quotation_subject, Eligibility Determination, Public Policy, Disease, Health Services Accessibility, Social Security, Cost of Illness, Alzheimer Disease, Risk Factors, medicine, Prevalence, Dementia, Homes for the Aged, Humans, Ethics, Medical, Young adult, Survival rate, Biological Psychiatry, media_common, Aged, Public health, Dementia, Vascular, Age Factors, Art, Caregiver burden, Middle Aged, medicine.disease, Nursing Homes, Survival Rate, Neuropsychology and Physiological Psychology, Caregivers, Frontotemporal Dementia, Ethnology, Female, Neurology (clinical), France, Geriatrics and Gerontology, Alzheimer's disease
Abstract

The number of patients with young onset dementia (YOD) (that is before age 65) is estimated at 32,000 in France, and 5000 with onset dementia before 60 years. These patients differ from older ones by the greater number of rares causes (29%), heterogeneity of the presentation among the usual diseases, such as non-amnestic phenotypes of Alzheimer's disease, high frequency of frontal symptoms, and possible genetic origin. These aspects must be taken into account for the diagnosis, often more difficult than in older ones because patients have a little knowledge of the YOD, excepted in the genetics forms. YOD patients can still work or drive a car, and we should choose between the respect for autonomy and the security for the patient and their carers. YOD patients can be more often included in pharmacological trials because they have lower associated disorders. Individual non-pharmacological treatment should be priviledged because they don't easily accept collective activities with other patients over 60 years of age. Excepted for the very young patients (onset before 45), the survival is longer than in late onset dementia, with sometimes severe behavioral problems related to frontal syndrome. In France, the caregiving at home has been improved since the possibility for the YOD patients to receive a financial assistance reserved for the disabled patients, but admission to a nursing home before 60 is very difficult and increases the caregiver burden and perception of unfairness. There is a discrimination between young or older demented patients related to the great difficulty to meet the needs of younger patients, due to the rigidity of the medical and social systems. The presentation of a limited offer for the YOD patients must initiate reflections on our capacities to respect the autonomy and the dignity of the Alzheimer's patients regardless of age.

Published
2012

49. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain

Author

H. Hattig, C. Delli Pizzi, M. C. Addonizio, Michelle Davis, A. R. Giovagnoli, L. Florensa, M. Roth, J. de Kruijk, Francisco Lacruz, Ph. Dewailly, A. Toygar, C. Avendano, P.P. De Deyn, J. F. Hurtevent, F. Lomeila, T. W. Wong, Gordon T. Plant, M. Bud, H. J. Willison, DH Miller, D. W. Langdon, R. Cioni, J. Servan, A. Kaygisiz, E. Racadot, D. B. Schens, E. Picciola, L. Falip, C. Bouchard, J. Jotova, A. Jorge-Santamaria, P. Misra, A. Dufour, C. P. Panagopoulos, A. Venneri, B. Sredni, B. Angelard, M. Janelidze, M. Carreno, J. Obenberger, J. Pouget, H. W. Moser, R. Kaufmann, J. A. Molina, D. Linden, A. Martin Urda, E. Uvestad, A. Krone, J. P. Cochin, J. Mallecourt, A. Cambon-Thomsen, K. Violleau, P. Osschmann, A. M. Durocher, E. Bussaglia, D. M. Danielle, H. Efendi, C. Van Broeckhoven, K. G. Jordan, W. Rautenberg, C. Iniguez, J. M. Delgado, Graham Watson, M. Lawden, Gareth J. Barker, K. Stiasny, James T. Becker, G. Campanella, E. Peghi, A. Poli, A. Haddad, T. Yamawaki, Giacomo P. Comi, S. Sotgiu, B. Ersmark, A. Pomes, M. Ziegler, P. Ferrante, P. Ruppi, H. KuÇukoglu, R. Bouton, U. K. Rinne, P. Vieregge, M. Dary, P. Giunti, Peter J. Goadsby, S. Jung, E. Secor, A. Steinberg, N. Vila, M. A. Hernandez, M. Cursi, A. Enqelhardt, A. Engelhardt, J. Veitch, F. Di Silverio, F. Arnaud, B. Neundörfer, R. Brucher, Dominique Caparros-Lefebvre, B. Meyer, Marianne Dieterich, M. H. Snidaro, R. Gomez, R. Cerbo, M. Ragno, J. M. Vance, S. Nemni, A. Caliskan, F. Barros, I. Velcheva, D. Ceballos-Baumann, V. Barak, A. Avila, N. Antonova, F. Resche, S. Pappata, L. Varela, S. R. Silveira Santos, A. Cammarota, L. Naccache, Y. Nara, E. Tournier-Lasserves, R. Mobner, T. Chase, A. Ensenyat, J. Ulrich, G. Giegerich, M. Rother, M. Revilla, N. Nitschke, K. Honczarenko, E. Basart Tarrats, J. Blin, B. Jacob, J. Santamaria, S. Knezevic, J. L. Castillo, M. Antem, J. Colomer, O. Busse, Didier Hannequin, S. Carrier, J. B. Ruidavets, C. Rozman, J. Bogoussslavsky, J. Pascual Calvet, E. Monros, J. M. Polo, M. 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Lane, A. Hofman, M. Verin, T. Matilla, P. Bedoucha, J. Roche, M. Lai, M. Collard, A. Ugarte, F. Gallecho, D. Silbersweig, C. Kennard, J. P. Azulay, T. W. Ho, P. L. I. Dellemijn, R. Girardello, F. Baas, B. Voss, F. Rozenberg, E. M. Brocker, V. Stanev, A. A. J. Soeterboek, A. Marra, A. Rey, E. Ertem, M. Sawradewicz-Rybak, J. De Keyser, P. Cavallari, F. Proust, Y. Chevalier, H. C. Hansen, D. Leys, C. A. Davie, K. Hoang-Xuan, C. Bairati, H. van Crevel, Thomas T. Warner, B. Bompais, A. Dobbeleir, T Campbell, C. Macko, C. J. M. Klijn, M. Dussallant, T. P. Berlit, W. Rozenbaum, M. J. van den Bent, W. A. Rocca, M. Muller, H. Hundemer, U. Zifko, M. Campera, F. Drislane, D. Ranoux, T. M. Kloss, Anil Kumar, I. Ruolt, C. Bargnani, B. Marescau, N. A. Losseff, S. Notermans, B. Kint, E. T. Burke, C. Aykut, J. Matias Guiu, P. Maquet, T. Drogendijk, M. Leone, K. von Ammon, M. Pepeliarska, C. Prados, L. DiGiamberardino, T. Logtenberg, G. Lenoir, I. Castaldo, Damhaut, M. Radionova, G. Sirabian, R. 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Subjects
Neurology, business.industry, Media studies, Library science, Medicine, Neurology (clinical), business
Published
1994
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50. SPECT Data in a Case of Secondary Capgras Delusion

Author

D. Caparros-Lefebvre, Florence Pasquier, Cabaret M, Florence Lebert, Marc Steinling, and Henri Petit

Subjects
Adult, medicine.medical_specialty, Neurocognitive Disorders, Neuropsychological Tests, Neuropsychiatry, Lesion, Delusion, Parietal Lobe, medicine, Humans, Dominance, Cerebral, Psychiatry, Cerebral Cortex, Tomography, Emission-Computed, Single-Photon, Brain Mapping, Capgras delusion, medicine.diagnostic_test, Cerebral Palsy, Multiple sclerosis, medicine.disease, Psychiatry and Mental health, Clinical Psychology, Capgras Syndrome, Positron emission tomography, Female, Radiology, medicine.symptom, Psychology
Abstract

Capgras' delusion (CD) may be secondary to a neurologic lesion, particularly in the right frontal or occipital regions. A 40-year-old woman with multiple sclerosis underwent SPECT during and after an episode of CD. Analysis during delusion showed an uptake defect in the right parietal cortex with an 11% index of asymmetry (normal:or = 4%). Post-delusion SPECT showed decreased bifrontal and biparietal cortical uptake indices but a normal index of asymmetry. Functional brain imaging may provide clues to the psychopathology of CD.

Published
1994
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