Search

Your search keyword '"Albert Puig-Pijoan"' showing total 16 results
Start Over Author "Albert Puig-Pijoan" Search Limiters Available in Library Collection
16 results on '"Albert Puig-Pijoan"'

1. Plasma brain-derived tau is an amyloid-associated neurodegeneration biomarker in Alzheimer’s disease

Author

Fernando Gonzalez-Ortiz, Bjørn-Eivind Kirsebom, José Contador, Jordan E. Tanley, Per Selnes, Berglind Gísladóttir, Lene Pålhaugen, Mathilde Suhr Hemminghyth, Jonas Jarholm, Ragnhild Skogseth, Geir Bråthen, Gøril Grøndtvedt, Atle Bjørnerud, Sandra Tecelao, Knut Waterloo, Dag Aarsland, Aida Fernández-Lebrero, Greta García-Escobar, Irene Navalpotro-Gómez, Michael Turton, Agnes Hesthamar, Przemyslaw R. Kac, Johanna Nilsson, Jose Luchsinger, Kathleen M. Hayden, Peter Harrison, Albert Puig-Pijoan, Henrik Zetterberg, Timothy M. Hughes, Marc Suárez-Calvet, Thomas K. Karikari, Tormod Fladby, and Kaj Blennow

Subjects
Science
Abstract

Abstract Staging amyloid-beta (Aβ) pathophysiology according to the intensity of neurodegeneration could identify individuals at risk for cognitive decline in Alzheimer’s disease (AD). In blood, phosphorylated tau (p-tau) associates with Aβ pathophysiology but an AD-type neurodegeneration biomarker has been lacking. In this multicenter study (n = 1076), we show that brain-derived tau (BD-tau) in blood increases according to concomitant Aβ (“A”) and neurodegeneration (“N”) abnormalities (determined using cerebrospinal fluid biomarkers); We used blood-based A/N biomarkers to profile the participants in this study; individuals with blood-based p-tau+/BD-tau+ profiles had the fastest cognitive decline and atrophy rates, irrespective of the baseline cognitive status. Furthermore, BD-tau showed no or much weaker correlations with age, renal function, other comorbidities/risk factors and self-identified race/ethnicity, compared with other blood biomarkers. Here we show that blood-based BD-tau is a biomarker for identifying Aβ-positive individuals at risk of short-term cognitive decline and atrophy, with implications for clinical trials and implementation of anti-Aβ therapies.

Published
2024
Full Text
View/download PDF

2. Medical help-seeking intentions among patients with early Alzheimer’s disease

Author

Alberto Villarejo-Galende, Elena García-Arcelay, Gerard Piñol-Ripoll, Antonio del Olmo-Rodríguez, Félix Viñuela, Mercè Boada, Emilio Franco-Macías, Almudena Ibañez de la Peña, Mario Riverol, Albert Puig-Pijoan, Pedro Abizanda-Soler, Rafael Arroyo, Miquel Baquero-Toledo, Inmaculada Feria-Vilar, Mircea Balasa, Ángel Berbel, Eloy Rodríguez-Rodríguez, Alba Vieira-Campos, Guillermo Garcia-Ribas, Silvia Rodrigo-Herrero, Alberto Lleó, and Jorge Maurino

Subjects
Alzheimer’s disease, help-seeking, early diagnosis, illness representation, awareness, Psychiatry, RC435-571
Abstract

BackgroundLimited information is available on the active process of seeking medical help in patients with Alzheimer’s disease (AD) at early stages. The aim of this study was to assess the phenomenon of medical help-seeking in early AD and to identify associated factors.MethodsA multicenter, non-interventional study was conducted including patients of 50–90 years of age with prodromal or mild AD (National Institute on Aging/Alzheimer’s Association criteria), a Mini-Mental State Examination (MMSE) score ≥ 22, and a Clinical Dementia Rating-Global score (CDR-GS) of 0.5–1.0. A multivariate logistic regression analysis was conducted.ResultsA total of 149 patients were included. Mean age (SD) was 72.3 (7.0) years, 50.3% were female, and 87.2% had a CDR-GS score of 0.5. Mean disease duration was 1.4 (1.8) years. Ninety-four (63.1%) patients sought medical help, mostly from neurologists. Patients with help-seeking intentions were mostly female (60.6%) with a CDR-GS score of 0.5 (91.5%) and had a greater awareness of diagnosis, poorer quality of life, more depressive symptoms, and a more severe perception of their condition than their counterparts. Lack of help-seeking intentions was associated with male sex (p = 0.003), fewer years of education (p = 0.005), a low awareness of diagnosis (p = 0.005), and a low emotional consequence of the condition (p = 0.016).ConclusionUnderstanding the phenomenon of active medical help-seeking may facilitate the design of specific strategies to improve the detection of cognitive impairment, especially in patients with a lower level of educational attainment and poor awareness of their condition.

Published
2023
Full Text
View/download PDF

3. Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts

Author

Juan Lantero-Rodriguez, Agathe Vrillon, Aida Fernández-Lebrero, Paula Ortiz-Romero, Anniina Snellman, Laia Montoliu-Gaya, Wagner S. Brum, Emmanuel Cognat, Julien Dumurgier, Albert Puig-Pijoan, Irene Navalpotro-Gómez, Greta García-Escobar, Thomas K. Karikari, Eugeen Vanmechelen, Nicholas J. Ashton, Henrik Zetterberg, Marc Suárez-Calvet, Claire Paquet, and Kaj Blennow

Subjects
Alzheimer’s disease, CSF, Biomarkers, p-tau235, p-tau181, p-tau217, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings.

Published
2023
Full Text
View/download PDF

4. Blood Biomarkers of Alzheimer’s Disease and Cognition: A Literature Review

Author

Greta Garcia-Escobar, Rosa Maria Manero, Aida Fernández-Lebrero, Angel Ois, Irene Navalpotro-Gómez, Victor Puente-Periz, José Contador-Muñana, Isabel Estragués-Gazquez, Albert Puig-Pijoan, and Joan Jiménez-Balado

Subjects
Alzheimer’s disease, cognitive impairment, blood biomarkers, cognitive functions, cognition, Microbiology, QR1-502
Abstract

Recent advances in blood-based biomarkers of Alzheimer’s Disease (AD) show great promise for clinical applications, offering a less invasive alternative to current cerebrospinal fluid (CSF) measures. However, the relationships between these biomarkers and specific cognitive functions, as well as their utility in predicting longitudinal cognitive decline, are not yet fully understood. This descriptive review surveys the literature from 2018 to 2023, focusing on the associations of amyloid-β (Aβ), Total Tau (t-Tau), Phosphorylated Tau (p-Tau), Neurofilament Light (NfL), and Glial Fibrillary Acidic Protein (GFAP) with cognitive measures. The reviewed studies are heterogeneous, varying in design and population (cognitively unimpaired, cognitively impaired, or mixed populations), and show results that are sometimes conflicting. Generally, cognition positively correlates with Aβ levels, especially when evaluated through the Aβ42/Aβ40 ratio. In contrast, t-Tau, p-Tau, Nfl, and GFAP levels typically show a negative correlation with cognitive performance. While p-Tau measures generally exhibit stronger associations with cognitive functions compared to other biomarkers, no single blood marker has emerged as being predominantly linked to a specific cognitive domain. These findings contribute to our understanding of the complex relationship between blood biomarkers and cognitive performance and underscore their potential utility in clinical assessments of cognition.

Published
2024
Full Text
View/download PDF

5. Effects of COVID-19 Pandemic Confinement in Patients With Cognitive Impairment

Author

Ainara Barguilla, Aida Fernández-Lebrero, Isabel Estragués-Gázquez, Greta García-Escobar, Irene Navalpotro-Gómez, Rosa María Manero, Víctor Puente-Periz, Jaume Roquer, and Albert Puig-Pijoan

Subjects
COVID- 19, SARS - CoV-2, dementia, depression, cognitive impairment, anxiety, Neurology. Diseases of the nervous system, RC346-429
Abstract

Introduction: State of emergency caused by COVID-19 pandemic and subsequent lockdown hit Spain on 14th March 2020 and lasted until 21st June 2020. Social isolation measures were applied. Medical attention was focused on COVID-19. Primary and social care were mainly performed by telephone. This exceptional situation may affect especially vulnerable patients such as people living with dementia. Our aim was to describe the influence of restrictive measures on patients living with mild cognitive decline and dementia evaluating SARS-CoV2 infection, changes in routines, cognitive decline stage, neuropsychiatric symptoms, delirium, falls, caregiver stress, and access to sanitary care.Materials and Methods: We gathered MCI and dementia patients with clinical follow-up before and after confinement from DegMar registry (Hospital del Mar). A telephone ad-hoc questionnaire was administered. Global status was assessed using CDR scale. Changes in neuropsychiatric symptoms were assessed by Neuropsychiatric Inventory (NPI) and retrospective interview for pre-confinement base characteristics.Results: We contacted a total of 60 patients, age 75.4 years ± 5,192. 53.3% were women. Alzheimer's Disease (41.7%) and Mild Cognitive Impairment (25%) were the most prevalent diagnosis. Remaining cases included different dementia disorders. A total of 10% of patients had been diagnosed with SARS-CoV-2. During confinement 70% of patients abandoned previous daily activities, 60% had cognitive worsening reported by relatives/caretakers, 15% presented delirium episodes, and 13% suffered increased incidence of falls. Caregivers reported an increased burden in 41% cases and burnout in 11% cases. 16% reported difficulties accessing medical care, 33% received medical phone assistance, 20% needed emergency care and 21% had changes in psychopharmacological therapies. Neuropsychiatric profile globally worsened (p < 0.000), also in particular items like agitation (p = 0.003), depression (p < 0.000), anxiety (p < 0.000) and changes in appetite (p = 0.004).Conclusion: SARS-CoV2-related lockdown resulted in an important effect over social and cognitive spheres and worsening of neuropsychiatric traits in patients living with mild cognitive decline and dementia. Although the uncertainty regarding the evolution of the pandemic makes strategy difficult, we need to reach patients and caregivers and develop adequate strategies to reinforce and adapt social and health care.

Published
2020
Full Text
View/download PDF

6. Effects of COVID-19 Home Confinement on Mental Health in Individuals with Increased Risk of Alzheimer’s Disease

Author

Anna Soteras, José María González de Echevarri Gómez, Karine Fauria, From Bbrc, Rafael de la Torre, Laura Forcano, José Luis Molinuevo, Anna Boronat, Iva Knezevic, Nieves Pizarro, Iris Piera, Albert Puig-Pijoan, Thais Lorenzo, Julian Mateus, and Natalia Soldevila-Domenech

Subjects
Male, Risk, Short Communication, Apolipoprotein E4, Apolipoprotein E3, Disease, Psychological Distress, 03 medical and health sciences, 0302 clinical medicine, Alzheimer Disease, Humans, Medicine, Cognitive Dysfunction, Cognitive decline, Pathological, Depression (differential diagnoses), Aged, Aged, 80 and over, Depressive Disorder, 030214 geriatrics, business.industry, General Neuroscience, COVID-19, Cognition, General Medicine, Middle Aged, Anxiety Disorders, Mental health, Psychiatry and Mental health, Clinical Psychology, Mood, Spain, Quarantine, Subjective cognitive decline, Anxiety, Female, Geriatrics and Gerontology, medicine.symptom, Cognition Disorders, business, Alzheimer’s disease, 030217 neurology & neurosurgery, Confinement, Clinical psychology
Abstract

We explored the impact of the Spanish COVID-19 strict home confinement on mental health and cognition in non-infected subjects (N = 16, 60–80 years) diagnosed with subjective cognitive decline and APOE ɛ3/ɛ4 carriers. Mental health was monitored for 2 months on a daily, weekly, or monthly basis, and compared to pre-confinement values. Emotional distress, anxiety, and depression scores increased to pathological threshold values during and after confinement. Those with lower mood during confinement experienced a decline in their mood after confinement. Cognition did not change. These preliminary results suggest that mental health consequences of corona measures in preclinical stages of Alzheimer’s disease should be further evaluated.

Published
2021

7. Awareness of Diagnosis in Persons with Early-Stage Alzheimer's Disease: An Observational Study in Spain

Author

Alberto Villarejo-Galende, Elena García-Arcelay, Gerard Piñol-Ripoll, Antonio del Olmo-Rodríguez, Félix Viñuela, Mercè Boada, Emilio Franco-Macías, Almudena Ibañez de la Peña, Mario Riverol, Albert Puig-Pijoan, Pedro Abizanda-Soler, Rafael Arroyo, Miquel Baquero-Toledo, Inmaculada Feria-Vilar, Mircea Balasa, Ángel Berbel, Eloy Rodríguez-Rodríguez, Alba Vieira-Campos, Guillermo García-Ribas, Silvia Rodrigo-Herrero, Albert Lleó, Jorge Maurino, Roche, Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (España), European Commission, European Federation of Pharmaceutical Industries and Associations, Instituto de Salud Carlos III, Grifols, and Fundación 'la Caixa'

Subjects
Quality of life, Neurology, Well-being, Diagnosis, Neurology (clinical), Alzheimer's disease, Awareness, Illness representation, Alzheimer’s disease
Abstract

[Introduction] Limited information is available on people’s experiences of living with Alzheimer’s disease (AD) at earlier stages. This study assessed awareness of diagnosis among people with early-stage AD and its impact on different person-centered outcome measures., [Methods] We conducted an observational, cross-sectional study in 21 memory clinics in Spain. Persons aged 50–90 years, diagnosed with prodromal or mild AD (NIA/AA criteria), a Mini Mental State Examination (MMSE) score ≥ 22, and a Clinical Dementia Rating-Global score (CDR-GS) of 0.5 or 1.0 were recruited. The Representations and Adjustment to Dementia Index (RADIX) was used to assess participants’ beliefs about their condition and its consequences., [Results] A total of 149 persons with early-stage AD were studied. Mean (SD) age was 72.3 (7.0) years and 50.3% were female. Mean duration of AD was 1.4 (1.8) years. Mean MMSE score was 24.6 (2.1) and 87.2% had a CDR-GS score of 0.5. Most participants (n = 84, 57.5%) used a descriptive term related to specific AD symptoms (e.g., memory difficulties) when asked what they called their condition. Participants aware of their diagnosis using the term AD (n = 66, 45.2%) were younger, had more depressive symptoms, and poorer life satisfaction and quality of life compared to those without awareness of their specific diagnosis. Practical and emotional consequences RADIX scores showed a significant negative correlation with Quality of Life in Alzheimer’s Disease score (rho = − 0.389 and − 0.413, respectively; p, [Conclusions] Awareness of diagnosis was a common phenomenon in persons with early-stage AD negatively impacting their quality of life. Understanding illness representations in earlier stages may facilitate implementing optimized care that supports improved quality of life and well-being., This study was funded by the Medical Department of Roche Farma Spain (ML42346); funding sources with Life Molecular Imaging, Bioiberica, and Schwabe; and grants from CIBERNED, EU/EFPIA, Instituto de Salud Carlos III (ISCIII), Fundación La Caixa, and Grífols.

Published
2022

8. Quality of Life and the Experience of Living with Early-Stage Alzheimer's Disease

Author

Alberto Villarejo-Galende, Elena García-Arcelay, Gerard Piñol-Ripoll, Antonio del Olmo-Rodríguez, Félix Viñuela, Mercè Boada, Emilio Franco-Macías, Almudena Ibañez de la Peña, Mario Riverol, Albert Puig-Pijoan, Pedro Abizanda-Soler, Rafael Arroyo, Miquel Baquero-Toledo, Inmaculada Feria-Vilar, Mircea Balasa, Ángel Berbel, Eloy Rodríguez-Rodríguez, Alba Vieira-Campos, Guillermo García-Ribas, Silvia Rodrigo-Herrero, Ángeles Terrancle, Daniel Prefasi, Alberto Lleó, Jorge Maurino, Universidad de Cantabria, and Roche

Subjects
Quality of life, Amyloid, Early-stage, tau proteins, cerebrospinal fluid, White matter lesions, Magnetic resonance imaging, Alzheimer Disease, Surveys and Questionnaires, White matter hyperintensities, magnetic resonance imaging, Tau proteins, Humans, Cognitive Dysfunction, Aged, Depression, General Neuroscience, white matter lesions, amyloid, biomarkers, General Medicine, white matter hyperintensities, Psychiatry and Mental health, Clinical Psychology, Stigma, Cerebrospinal fluid, Quality of Life, Hopelessness, Self Report, Geriatrics and Gerontology, Alzheimer’s disease, Biomarkers
Abstract

[Background] There is a need to better understand the experience of patients living with Alzheimer's disease (AD) in the early stages., [Objective] The aim of the study was to evaluate the perception of quality of life in patients with early-stage AD., [Methods] A multicenter, non-interventional study was conducted including patients of 50–90 years of age with prodromal or mild AD, a Mini-Mental State Examination (MMSE) score ≥22, and a Clinical Dementia Rating-Global score (CDR-GS) of 0.5.–1.0. The Quality of Life in Alzheimer ’s Disease (QoL-AD) questionnaire was used to assess health-related quality of life. A battery of self-report instruments was used to evaluate different psychological and behavioral domains. Associations between the QoL-AD and other outcome measures were analyzed using Spearman’s rank correlations., [Results] A total of 149 patients were included. Mean age (SD) was 72.3 (7.0) years and mean disease duration was 1.4 (1.8) years. Mean MMSE score was 24.6 (2.1). The mean QoL-AD score was 37.9 (4.5). Eighty-three percent (n = 124) of patients had moderate-to-severe hopelessness, 22.1% (n = 33) had depressive symptoms, and 36.9% (n = 55) felt stigmatized. The quality of life showed a significant positive correlation with self-efficacy and negative correlations with depression, emotional and practical consequences, stigma, and hopelessness., [Conclusion] Stigma, depressive symptoms, and hopelessness are frequent scenarios in AD negatively impacting quality of life, even in a population with short disease duration and minimal cognitive impairment., This study was funded by the Medical Department of Roche Farma Spain (ML42346).

Published
2022

9. Network analysis for studying the dynamics of affective symptoms and treatment adherence in APOE‐ɛ4 carriers with subjective cognitive decline following a multimodal intervention: Preliminary findings from the PENSA Study

Author

Natalia Soldevila‐Domenech, Laura Forcano, Anna Boronat, Thais Lorenzo, Iris Piera, Albert Puig‐Pijoan, Iva Knezevic, Karine Fauria, Jose Luis Molinuevo, and Rafael de la Torre

Subjects
Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Epidemiology, Health Policy, Neurology (clinical), Geriatrics and Gerontology
Published
2021

10. Spanish normative studies (NEURONORMA-Plus project): norms for the Wisconsin Card Sorting Test, the Modified Taylor Complex Figure, and the Ruff-Light Trail Learning Test

Author

B. Pereira-Cuitiño, R.M. Manero, M. Florido-Santiago, Gonzalo Sánchez-Benavides, C. Pérez-Enríquez, J. Piqué-Candini, Jordi Peña-Casanova, C. Arrondo-Elizarán, Albert Puig-Pijoan, L. Grau-Guinea, and G. García-Escobar

Subjects
Aprendizaje y memoria, Estudios normativos, Funciones ejecutivas, Regression analysis, Test (assessment), Wisconsin Card Sorting Test, Age groups, Normas, Healthy individuals, Test score, Normative, Raw score, Neurology (clinical), Psychology, Clinical psychology
Abstract

Data de publicació electrónica: 20-09-2021 Objetivo: ell presente estudio tiene como objetivo proporcionar normas y ajustes para edad, educación y género para el Wisconsin Card Sorting Test (WCST), la Figura Compleja Modificada de Taylor (FCMT) y el Ruff-Light Trail Learning Test (RULIT) como parte del proyecto NEURONORMA-Plus. método: la muestra consiste en 308 individuos cognitivamente sanos de entre 18 y 92 años. Se proporcionan tablas para convertir las puntuaciones brutas en puntuaciones escalares ajustadas por edad y ajustes por educación y género tras aplicar modelos de regresión independientes en 2 grupos de edad (< 50 y ≥ 50 años).Resultados: la edad tuvo un efecto negativo en el rendimiento en ambos grupos etarios. Observamos un efecto positivo de la educación en el rendimiento del WCST en el grupo más joven (< 50 años), y en todas las medidas del FCMT (con la excepción de la tarea de reconocimiento) en el grupo de mayor edad (≥ 50 años). La educación no influyó en el rendimiento en el RULIT, pero sí el género, que tuvo un efecto leve, aunque significativo, mostrando los hombres jóvenes un mayor rendimiento en una variable. conclusión: los datos normativos aportados pueden contribuir en la interpretación clínica del rendimiento en estas pruebas en población española.

Published
2021

11. International initiative for harmonization of cerebrospinal fluid diagnostic comments in Alzheimer's disease

Author

Mari L DeMarco, Clementine Gondolf, Léonor Nogueira, Michael Khalil, Koen Poesen, Aurélie Bedel, Andreas Jeromin, Marie-Céline Blanc, Daniel Alcolea, Markus Otto, Agnieszka Kulczyńska-Przybik, Marc Suárez-Calvet, Benoit Rucheton, Muriel Quillard-Muraine, Hermann Esselmann, Maria Bjerke, Alberto Lleó, Anne Fogli, Frédérique Grandhomme, Olivier Bousiges, Federico Verde, M D'Onofrio, Oriol Grau-Rivera, Ashvini Keshavan, Hayrettin Tumani, Melanie Hart, Isabelle Quadrio, Sylvain Lehmann, Albert Puig‐Pijoan, Lucie Vaudran, Marcel M. Verbeek, Lucilla Parnetti, Peter Koertvelyessy, Catherine Malaplate, Armand Perret-Liaudet, Henrik Zetterberg, Jens Wiltfang, Lisa Vermunt, Chinedu T. Udeh-Momoh, Katell Poec, Claire Paquet, Magda Tsolaki, Barbara Mroszko, Jean-Baptiste Oudart, Jean-Louis Laplanche, Sebastiaan Engelborghs, Miles D. Chapman, Elodie Bouaziz Amar, Jonathan Vogelgsang, Susanna Schraen, Edith Bigot-Corbel, Elisabetta Galloni, Adelina Orellana, Constance Delaby, Anne Beaume, Diane Dufour-Rainfray, and Charlotte E. Teunissen

Subjects
medicine.medical_specialty, Epidemiology, business.industry, Health Policy, Harmonization, Disease, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Cerebrospinal fluid, Developmental Neuroscience, medicine, Neurology (clinical), Geriatrics and Gerontology, Intensive care medicine, business
Published
2020

12. A co‐creation approach to design the implementation of a multimodal intervention in patients with subjective cognitive decline (PENSA study)

Author

José Luis Molinuevo, Iva Knezevic, Maria Dolores Rodriguez‐Arjona, Karine Fauria, Albert Puig‐Pijoan, Carolina Minguillon, Natalia Soldevila-Domenech, Laura Forcano, and Nieves Pizarro

Subjects
Gerontology, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Epidemiology, Health Policy, Intervention (counseling), Co-creation, In patient, Neurology (clinical), Geriatrics and Gerontology, Cognitive decline, Psychology
Published
2020

13. PENSA study: Study design, recruitment profiles and participant inclusion in multimodal intervention studies

Author

Gonzalo Sánchez-Benavides, Anna Boronat, Rafael de la Torre, Albert Puig-Pijoan, Natalia Soldevila-Domenech, Sofia Menezes-Cabral, Carolina Minguillon, José Luis Molinuevo, Aida Cuenca, Julian Mateus, Iva Knezevic, Karine Fauria, Juan Domingo Gispert, and Laura Forcano

Subjects
Psychiatry and Mental health, Cellular and Molecular Neuroscience, medicine.medical_specialty, Developmental Neuroscience, Epidemiology, Health Policy, Physical therapy, medicine, Neurology (clinical), Geriatrics and Gerontology, Psychology, Intervention studies, Inclusion (education)
Published
2020

14. One-Year Reference Norms of Cognitive Change in Spanish Old Adults: Data from the NEURONORMA Sample

Author

Anna Frank-García, R.M. Manero, Carmen Antúnez, Rafael Blesa, Manuel Fernández-Martínez, Albert Puig-Pijoan, Nina Gramunt, Miguel Aguilar, Neuronorma Study Team, Alfredo Robles, M. Casals-Coll, J. Peña-Casanova, and Gonzalo Sánchez-Benavides

Subjects
Male, 050103 clinical psychology, medicine.medical_specialty, Aging, Sample (statistics), Neuropsychological Tests, 03 medical and health sciences, 0302 clinical medicine, Cognition, Reference Values, medicine, Humans, 0501 psychology and cognitive sciences, Longitudinal Studies, Cognitive decline, Geriatric Assessment, Aged, Geriatrics, Aged, 80 and over, 05 social sciences, Neuropsychology, General Medicine, Middle Aged, Cognitive test, Psychiatry and Mental health, Clinical Psychology, Neuropsychology and Physiological Psychology, Spain, Normative, Observational study, Female, Psychology, Cognition Disorders, 030217 neurology & neurosurgery, Clinical psychology
Abstract

Objective Serial cognitive assessments are useful for many purposes, such as monitoring cognitive decline or evaluating the result of an intervention. In order to determine if an observed change is reliable and meaningful, longitudinal reference data from non-clinical samples are needed. Since neuropsychological outcomes are affected by language and cultural background, cognitive tests should be adapted, and country-based norms collected. The lack of cross-sectional normative data for Spanish population has been partially remediated, but there is still a need of reliable change norms. This paper aims to give an initial response to this need by providing several reliable change indices (RCI) for 1-year follow-up in a Spanish sample. Method A longitudinal observational study was designed. A total of 122 healthy subjects over age 50 were evaluated twice (M = 369.5, SD= 10.7 days) with the NEURONORMA battery. Scores changes were analyzed, and simple discrepancy scores, standard deviation indices, RCI, and standardized regression-based scores were calculated. Results Significant improvements were observed in variables related to memory, both verbal and visual, visuospatial function, and the completion time of complex problems. Reference tables for several RCI are provided for their use in clinical settings. Conclusions Our results confirm the existence of heterogeneous practice effects after 1 year, and support the recommendation of using reliable change norms to avoid misdiagnosis in repeated assessments. This study provides with initial, preliminary norms of cognitive change for its use in Spanish elders. Further studies on larger samples and different inter-visit intervals are still needed.

Published
2016

15. The antigen-binding fragment of human gamma immunoglobulin prevents amyloid β-peptide folding into β-sheet to form oligomers

Author

Ernest Palomer, Xavier Fernàndez-Busquets, Marta Sabariego Puig, Rubén Vicente, Jaume Bonet, Albert Puig-Pijoan, Alex Perálvarez-Marín, Francisco J. Muñoz, Xavier Altafaj, Baldomero Oliva, Marta Tajes, Biuse Guivernau, and Victòria Valls-Comamala

Subjects
0301 basic medicine, Models, Molecular, Protein Folding, Beta sheet, Protein Structure, Secondary, chemistry.chemical_compound, 0302 clinical medicine, Medicine, Immunoglobulin Fragments, Neurons, biology, Atomic force microscopy, Malalties neurodegeneratives, Neurodegenerative diseases, amyloid, Alzheimer's disease, Amyloid β peptide, Neuroprotective Agents, Oncology, Thioflavin, Antibody, Alzheimer’s disease, Protein Binding, Research Paper, Amyloid, Immunoglobulin gamma-Chains, Immunoglobulins, Protein Aggregation, Pathological, 03 medical and health sciences, Protein Aggregates, Alzheimer Disease, mental disorders, Immunoglobulin, Humans, Fab, Antigens, oligomers, Antigen Binding Fragment, Amyloid beta-Peptides, business.industry, Cortical neurons, Molecular biology, 030104 developmental biology, Malaltia d'Alzheimer, chemistry, Oligomers, biology.protein, Protein Multimerization, business, Immunoglobulines, immunoglobulin, 030217 neurology & neurosurgery
Abstract

// Victoria Valls-Comamala 1 , Biuse Guivernau 1 , Jaume Bonet 2 , Marta Puig 1 , Alex Peralvarez-Marin 3 , Ernest Palomer 1 , Xavier Fernandez-Busquets 4, 5 , Xavier Altafaj 6 , Marta Tajes 7 , Albert Puig-Pijoan 8 , Ruben Vicente 1 , Baldomero Oliva 2 and Francisco J. Munoz 1 1 Laboratory of Molecular Physiology, Faculty of Health and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain 2 Laboratory of Structural Bioinformatics (GRIB), Faculty of Health and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain 3 Unitat de Biofisica, Departament de Bioquimica i de Biologia Molecular, Facultat de Medicina, Universitat Autonoma de Barcelona, Barcelona, Spain 4 Institute for Bioengineering of Catalonia (IBEC), Barcelona, Spain 5 ISGlobal, Barcelona Centre for International Health Research, Hospital Clinic-Universitat de Barcelona, Barcelona, Spain 6 Bellvitge Biomedical Research Institute (IDIBELL) - Unit of Neuropharmacology and Pain, University of Barcelona, Barcelona, Spain 7 Heart Diseases Biomedical Research Group, IMIM-Hospital del Mar Medical Research Institute, Barcelona, Spain 8 Servei de Neurologia, Hospital del Mar-IMIM-Parc de Salut Mar, Barcelona, Spain Correspondence to: Francisco J. Munoz, email: paco.munoz@upf.edu Keywords: Alzheimer’s disease, amyloid, immunoglobulin, Fab, oligomers Received: December 22, 2016 Accepted: March 22, 2017 Published: April 13, 2017 ABSTRACT The amyloid beta-peptide (Aβ) plays a leading role in Alzheimer’s disease (AD) physiopathology. Even though monomeric forms of Aβ are harmless to cells, Aβ can aggregate into β-sheet oligomers and fibrils, which are both neurotoxic. Therefore, one of the main therapeutic approaches to cure or delay AD onset and progression is targeting Aβ aggregation. In the present study, we show that a pool of human gamma immunoglobulins (IgG) protected cortical neurons from the challenge with Aβ oligomers, as assayed by MTT reduction, caspase-3 activation and cytoskeleton integrity. In addition, we report the inhibitory effect of IgG on Aβ aggregation, as shown by Thioflavin T assay, size exclusion chromatography and atomic force microscopy. Similar results were obtained with Palivizumab, a human anti-sincitial virus antibody. In order to dissect the important domains, we cleaved the pool of human IgG with papain to obtain Fab and Fc fragments. Using these cleaved fragments, we functionally identified Fab as the immunoglobulin fragment inhibiting Aβ aggregation, a result that was further confirmed by an in silico structural model. Interestingly, bioinformatic tools show a highly conserved structure able to bind amyloid in the Fab region. Overall, our data strongly support the inhibitory effect of human IgG on Aβ aggregation and its neuroprotective role.

16. Clinical reporting following the quantification of cerebrospinal fluid biomarkers in Alzheimer's disease: An international overview

Author

Constance Delaby, Charlotte E. Teunissen, Kaj Blennow, Daniel Alcolea, Ivan Arisi, Elodie Bouaziz Amar, Anne Beaume, Aurélie Bedel, Giovanni Bellomo, Edith Bigot‐Corbel, Maria Bjerke, Marie‐Céline Blanc‐Quintin, Mercè Boada, Olivier Bousiges, Miles D Chapman, Mari L. DeMarco, Mara D'Onofrio, Julien Dumurgier, Diane Dufour‐Rainfray, Sebastiaan Engelborghs, Hermann Esselmann, Anne Fogli, Audrey Gabelle, Elisabetta Galloni, Clémentine Gondolf, Frédérique Grandhomme, Oriol Grau‐Rivera, Melanie Hart, Takeshi Ikeuchi, Andreas Jeromin, Kensaku Kasuga, Ashvini Keshavan, Michael Khalil, Peter Körtvelyessy, Agnieszka Kulczynska‐Przybik, Jean‐Louis Laplanche, Piotr Lewczuk, Qiao‐Xin Li, Alberto Lleó, Catherine Malaplate, Marta Marquié, Colin L. Masters, Barbara Mroczko, Léonor Nogueira, Adelina Orellana, Markus Otto, Jean‐Baptiste Oudart, Claire Paquet, Federico Paolini Paoletti, Lucilla Parnetti, Armand Perret‐Liaudet, Katell Peoc'h, Koen Poesen, Albert Puig‐Pijoan, Isabelle Quadrio, Muriel Quillard‐Muraine, Benoit Rucheton, Susanna Schraen, Jonathan M. Schott, Leslie M. Shaw, Marc Suárez‐Calvet, Magda Tsolaki, Hayrettin Tumani, Chinedu T Udeh‐Momoh, Lucie Vaudran, Marcel M Verbeek, Federico Verde, Lisa Vermunt, Jonathan Vogelgsang, Jens Wiltfang, Henrik Zetterberg, Sylvain Lehmann, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Universitat Autònoma de Barcelona (UAB), Hospital de la Santa Creu i Sant Pau, Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Amsterdam UMC - Amsterdam University Medical Center, Vrije Universiteit Amsterdam [Amsterdam] (VU), Sahlgrenska Academy at University of Gothenburg [Göteborg], European Brain Research Institute [Rome, Italy] (EBRI), Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre hospitalier universitaire de Poitiers (CHU Poitiers), CHU Bordeaux [Bordeaux], Università degli Studi di Perugia = University of Perugia (UNIPG), Centre hospitalier universitaire de Nantes (CHU Nantes), Vrije Universiteit Brussel (VUB), University of Antwerp (UA), Hôpital Cochin [AP-HP], Universitat Internacional de Catalunya [Barcelona] (UIC), Centro de Investigacion Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III [Madrid] (ISC), Laboratoire de Biochimie et de Biologie Moléculaire, CHU Strasbourg-Hôpital de Hautepierre [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), University of British Columbia (UBC), Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Imagerie et cerveau (iBrain - Inserm U1253 - UNIV Tours ), Université de Tours (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), University Medical Center Göttingen (UMG), CHU Clermont-Ferrand, CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), IMIM-Hospital del Mar, Generalitat de Catalunya, Niigata University, Medical University of Graz, Freie Universität Berlin, Humboldt University Of Berlin, Charité - UniversitätsMedizin = Charité - University Hospital [Berlin], German Research Center for Neurodegenerative Diseases - Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Medical University of Białystok (MUB), Universitätsklinikum Erlangen [Erlangen], Friedrich-Alexander Universität Erlangen-Nürnberg (FAU), The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Universität Ulm - Ulm University [Ulm, Allemagne], Matrice extracellulaire et dynamique cellulaire - UMR 7369 (MEDyC), Université de Reims Champagne-Ardenne (URCA)-SFR CAP Santé (Champagne-Ardenne Picardie Santé), Université de Reims Champagne-Ardenne (URCA)-Université de Reims Champagne-Ardenne (URCA)-Centre National de la Recherche Scientifique (CNRS), Centre de recherche en neurosciences de Lyon - Lyon Neuroscience Research Center (CRNL), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Hospices Civils de Lyon (HCL), Hôpital Beaujon [AP-HP], Catholic University of Leuven - Katholieke Universiteit Leuven (KU Leuven), CHU Rouen, Normandie Université (NU), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Sorbonne Université (SU), 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), Excellence Laboratory LabEx DISTALZ, University of Pennsylvania, Aristotle University of Thessaloniki, Imperial College London, Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Université de Lille, Radboud University Medical Center [Nijmegen], McLean Hospital [Belmont, Ma.], Harvard Medical School [Boston] (HMS), Universidade de Aveiro, Sahlgrenska University Hospital [Gothenburg], UK Dementia Research Institute (UK DRI), University College of London [London] (UCL), Institute of Neurology [London], Laboratory Medicine, Amsterdam Neuroscience - Neurodegeneration, Amsterdam Neuroscience - Neuroinfection & -inflammation, Neurology, Clinical Biology, Clinical sciences, and Neuroprotection & Neuromodulation

Subjects
Epidemiology, Neuroscience(all), [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Clinical Neurology, tau Proteins, cerebrospinal fluid [Amyloid beta-Peptides], Cellular and Molecular Neuroscience, Developmental Neuroscience, Alzheimer Disease, Humans, ddc:610, cerebrospinal fluid [Peptide Fragments], clinical report, cerebrospinal fluid biomarkers, consensus approach, Amyloid beta-Peptides, Health Policy, diagnosis [Alzheimer Disease], Alzheimer's disease, Disorders of movement Donders Center for Medical Neuroscience [Radboudumc 3], Peptide Fragments, cerebrospinal fluid [Alzheimer Disease], Psychiatry and Mental health, cerebrospinal fluid [Biomarkers], cerebrospinal fluid [tau Proteins], harmonization, Neurology (clinical), Human medicine, Geriatrics and Gerontology, Alzheimer’s disease, Biomarkers
Abstract

Introduction: the current practice of quantifying cerebrospinal fluid (CSF) biomarkers as an aid in the diagnosis of Alzheimer's disease (AD) varies from center to center. For a same biochemical profile, interpretation and reporting of results may differ, which can lead to misunderstandings and raises questions about the commutability of tests. Methods: We obtained a description of (pre-)analytical protocols and sample reports from 40 centers worldwide. A consensus approach allowed us to propose harmonized comments corresponding to the different CSF biomarker profiles observed in patients. Results: the (pre-)analytical procedures were similar between centers. There was considerable heterogeneity in cutoff definitions and report comments. We therefore identified and selected by consensus the most accurate and informative comments regarding the interpretation of CSF biomarkers in the context of AD diagnosis. Discussion: this is the first time that harmonized reports are proposed across worldwide specialized laboratories involved in the biochemical diagnosis of AD. This manuscript was facilitated by the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment (ISTAART), through the Biofluid Based Biomarkers Professional Interest Area (BBB-PIA). The views and opinions expressed in this publication represent those of the authors and do not necessarily reflect those of the BBB-PIA membership, ISTAART, or the Alzheimer's Association. The authors thank the French Society of Clinical Biology, the ISTAART BBB-PIA, and the Society for Neurochemistry and Clinical CSF analysis for their help in initiating this work. Constance Delaby received no support for the present manuscript. Charlotte Teunissen received the following grants during the last 36 months: Research of CET is supported by the European Commission (Marie Curie International Training Network, grant agreement No 860197 [MIRIADE], and JPND), Health Holland, the Dutch Research Council (ZonMw), Alzheimer Drug Discovery Foundation, The Selfridges Group Foundation, Alzheimer Netherlands, Alzheimer Association. CT and WF are recipients of ABOARD, which is a public-private partnership receiving funding from ZonMw (#73305095007) and Health∼Holland, Topsector Life Sciences & Health (PPP-allowance; #LSHM20106). More than 30 partners participate in ABOARD. ABOARD also receives funding from Edwin Bouw Fonds and Gieskes-Strijbisfonds. IV is appointed on a research grant by Alzheimer Nederland (NL-17004). She received no support for the present manuscript. Kaj Blennow is supported by the Swedish Alzheimer Foundation (#AF-742881) and Hjärnfonden, Sweden (#FO2017-0243). He received no support for the present manuscript. Daniel Alcolea received funding from Institute of Health Carlos III (ISCIII), Spain PI18/00435 and INT19/00016, and by the Department of Health Generalitat de Catalunya PERIS program SLT006/17/125. He received no support for the present manuscript. Ivan Arisi was partly supported by: Fondo Ordinario Enti (FOE D.M 865/2019) funds in the framework of a collaboration agreement between the Italian National Research Council and EBRI (2019-2021); POR (Operative Program Lazio Region, Italy) FESR (European Program Regional Development) 2014-2020, Public Notice “LIFE 2020” MODIAG Project. Elodie Bouaziz-Amar received no support for the present manuscript. Anne Beaume received no support for the present manuscript. Aurélie Bedel received no support for the present manuscript. Giovanni Bellomo is supported by University of Perugia, CIRMMP, IRST Istituto Romagnolo per lo Studio e la Cura dei Tumori, Innuvatech srl. He received no support for the present manuscript. Edith Bigot-Corbel received no support for the present manuscript. Maria Bjerke received no support for the present manuscript. Marie-Céline Blanc-Quintin received no support for the present manuscript. Mercè Boada received support from LA CAIXA, IMI, ISCIII H2020 the European Union/EFPIA Innovative Medicines Initiative Joint Undertaking MOPEAD project (Grants No. 115985) and is also supported by national grant, PI17/01474 from Acción Estratégica en Salud, integrated into the Spanish National Plan of R+D+I and founded by ISCIII (Instituto de Salud Carlos III)-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER- “Una manera de Hacer Europa”). She received no support for the present manuscript. Olivier Bousigues is supported by A2MCL Alsace Alzheimer. He received no support for the present manuscript. Miles D. Chapman received no support for the present manuscript. Mari L. DeMarco is supported by the Michael Smith Foundation for Health Research, Brain Canada (Canada Brain Research Fund), Health Canada, Women's Brain Health Initiative, Alzheimer Society of Canada, St. Paul's Foundation, Djavad Mowafaghian Centre for Brain Health at the University of British Columbia and the Canadian Consortium for Neurodegeneration and Aging; with all funds provided to the University of British Columbia. Mara D'Onofrio was partly supported by Fondo Ordinario Enti (FOE D.M 865/2019) funds in the framework of a collaboration agreement between the Italian National Research Council POR (Operative Program Lazio Region, Italy) FESR (European Program Regional Development) 2014-2020, Public Notice “LIFE 2020″, MODIAG Project. She received no support for the present manuscript. Julien Dumurgier received no support for the present manuscript. Diane Dufour received no support for the present manuscript. Sebastiaan Engelborghs is supported for various projects: Research Project GSKE/FMRE, Research Project FWO Vlaanderen, PhD fellowship FWO Vlaanderen (n = 3), VLAIO PhD fellowship. He received no support for the present manuscript. Hermann Esselmann received no support for the present manuscript. Anne Fogli received no support for the present manuscript. Audrey Gabelle received no support for the present manuscript. Elisabetta Galloni received no support for the present manuscript. Clémentine Gondolf received no support for the present manuscript. Frédérique Grandhomme received no support for the present manuscript. Oriol Grau-Rivera receives grants from the Spanish Ministry of Science, Innovation and Universities (FJCI-2017-33437), and from the Alzheimer's Association Research Fellowship Program (2019-AARF-644568). He received no support for the present manuscript. Melanie Hart receives UCLH Biomedical Research Centre support from NIHR (Neurosciences). She received no support for the present manuscript. Takeshi Ikeuchi received the following grants to his institution AMED: 21dk0207049, 21dk0207045, 21ek0109545, 20ek0109350, 20ek0109392. He received no support for the present manuscript. Andreas Jeromin received no support for the present manuscript. Kensaku Kasuga received no support for the present manuscript. Ashvini Keshavan is supported by the Weston Brain Institute/Selfridges Foundation grant UB170045. She received no support for the present manuscript. Michael Khalil received unrestricted research grants from Biogen and Novartis. He received no support for the present manuscript. Peter Körtvelyessy received no support for the present manuscript. Agnieszka Kulczynska-Przybik received no support for the present manuscript. Jean-Louis Laplanche received no support for the present manuscript. Qiao-Xin Li received no support for the present manuscript. Alberto Lleó is supported by grants from Generalitat de Catalunya (PERIS SLT002/16/00408), Instituto de Salud Carlos III (PI17/01896), Instituto de Salud Carlos III CIBERNED. He received no support for the present manuscript. Catherine Malaplate received no support for the present manuscript. Marta Marquié is supported by the Instituto de Salud Carlos III (ISCIII) Acción Estratégica en Salud, integrated in the Spanish National RCDCI Plan and financed by ISCIII-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER-Una manera de hacer Europa) grant PI19/00335. She received no support for the present manuscript. Colin M. Masters received no support for the present manuscript. Barbara Mroczko received a grant from The Binding Site Group and Biokom Diagnostyka. She received no support for the present manuscript. Léonor Nogueira received no support for the present manuscript. Adelina Orellana received no support for the present manuscript. Markus Otto is supported by BMBF, Thierry Latran foundation, EU, DFG. He received no support for the present manuscript. Jean-Baptiste Oudart is supported by Astrazeneca grant for a research program on EGFR targeted therapy resistance in NSCLC. He received no support for the present manuscript. Claire Paquet received no support for the present manuscript. Federico Paolini received no support for the present manuscript. Lucilla Parnetti received no support for the present manuscript. Armand Perret-Liaudet received no support for the present manuscript. Katell Peoc'h is supported by contract with Siemens Healthineers. She received no support for the present manuscript. Koen Poesen received no support for the present manuscript. Albert Puig-Pijoan received no support for the present manuscript. Isabelle Quadrio received no support for the present manuscript. Murielle Quillard-Muraine received no support for the present manuscript. Benoît Rucheton received no support for the present manuscript. Susanne Schraen received no support for the present manuscript. Jonathan M. Schott is supported by the Medical Research Council, Alzheimer's Research UK, Weston Brain Institute, British Heart Foundation, Alzheimer's Association. He received no support for the present manuscript. Leslie M. Shaw is supported by NIA for ADNI Biomarker Core, UPENN ADRC Biomarker Corr, MJ Fox PPMI for CSF Biomarker measurements, Roche for IIS study of AD biomarkers. He received no support for the present manuscript. Marc Suárez-Calvet receives funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (Grant agreement No. 948677). He also receives funding from the Instituto de Salud Carlos III (PI19/00155) and from the Spanish Ministry of Science, Innovation and Universities (Juan de la Cierva Programme grant IJC2018-037478-I). He received no support for the present manuscript. Magda Tsolaki received no support for the present manuscript. Hayrettin Tumani is supported by Alexion, Bayer, Biogen, Celgene, Genzyme-Sanofi, Merck, Novartis, Roche, Teva. He received no support for the present manuscript. Chinedu T Udeh-Momoh is supported by Alzheimer research UK (Project Grant). He received no support for the present manuscript. Lucie Vaudran received no support for the present manuscript. Marcel M. Verbeek is supported by the BIONIC project (no. 733050822, which has been made possible by ZonMw within the framework of “Memorabel,” the research and innovation program for dementia, as part of the Dutch national “Deltaplan for Dementia”: zonmw.nl/dementiaresearch), and the CAFÉ project (the National Institutes of Health, USA, grant number 5R01NS104147-02). The BIONIC project is a consortium of Radboudumc, LUMC, ADX Neurosciences, and University of Rhode Island University. MM Verbeek is also supported by a grant from the Selfridges Group Foundation. He received no support for the present manuscript. Federico Verde received no support for the present manuscript. Lisa Vermunt is supported by Alzheimer Nederland. She received no support for the present manuscript. Jonathan Volgesgang is supported by Clinician Scientist Research Fellowship, German Research Foundation (Deutsche Forschungsgesellschaft, project number: 413501650; 09/01/2019-02/28/2021); Eric Dorris Memorial Fellowship (McLean Hospital; 07/01/2020-06/30/2021). He received no support for the present manuscript. Jens Wiltfang is supported by Federal Ministry of Education and Research (BMBF) State of Lower Saxony; He received no support for the present manuscript. Henrik Zetterberg is a Wallenberg Scholar supported by grants from the Swedish Research Council (#2018-02532), the European Research Council (#681712), Swedish State Support for Clinical Research (#ALFGBG-720931), the Alzheimer Drug Discovery Foundation (ADDF), USA (#201809-2016862), the AD Strategic Fund and the Alzheimer's Association (#ADSF-21-831376-C, #ADSF-21-831381-C and #ADSF-21-831377-C), the Olav Thon Foundation, the Erling-Persson Family Foundation, Stiftelsen för Gamla Tjänarinnor, Hjärnfonden, Sweden (#FO2019-0228), the European Union's Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement No 860197 (MIRIADE), and the UK Dementia Research Institute at UCL. He received no support for the present manuscript. Sylvain Lehmann received no support for the present manuscript.

Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results