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1. Preclinical Alzheimer's disease: Definition, natural history, and diagnostic criteria.

Author

Dubois, Bruno, Hampel, Harald, Feldman, Howard H, Scheltens, Philip, Aisen, Paul, Andrieu, Sandrine, Bakardjian, Hovagim, Benali, Habib, Bertram, Lars, Blennow, Kaj, Broich, Karl, Cavedo, Enrica, Crutch, Sebastian, Dartigues, Jean-François, Duyckaerts, Charles, Epelbaum, Stéphane, Frisoni, Giovanni B, Gauthier, Serge, Genthon, Remy, Gouw, Alida A, Habert, Marie-Odile, Holtzman, David M, Kivipelto, Miia, Lista, Simone, Molinuevo, José-Luis, O'Bryant, Sid E, Rabinovici, Gil D, Rowe, Christopher, Salloway, Stephen, Schneider, Lon S, Sperling, Reisa, Teichmann, Marc, Carrillo, Maria C, Cummings, Jeffrey, Jack, Cliff R, Proceedings of the Meeting of the International Working Group (IWG) and the American Alzheimer's Association on “The Preclinical State of AD”, July 23, 2015, and Washington DC, USA

Subjects
Proceedings of the Meeting of the International Working Group (IWG) and the American Alzheimer's Association on “The Preclinical State of AD”, July 23, 2015, Washington DC, USA, Brain, Animals, Humans, Alzheimer Disease, Disease Progression, Alzheimer's disease, Amyloid PET, Asymptomatic, Biomarkers, Blood biomarkers, CSF biomarkers, Diagnostic criteria, Genetics, MRI, Pathophysiology, Preclinical, Tau PET, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Neurodegenerative, Dementia, Alzheimer's Disease, Brain Disorders, Acquired Cognitive Impairment, Human Genome, Neurosciences, Neurological, Clinical Sciences, Geriatrics
Abstract

During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum. Thanks to evolving biomarker research and substantial discoveries, it is now possible to identify the disease even at the preclinical stage before the occurrence of the first clinical symptoms. This preclinical stage of AD has become a major research focus as the field postulates that early intervention may offer the best chance of therapeutic success. To date, very little evidence is established on this "silent" stage of the disease. A clarification is needed about the definitions and lexicon, the limits, the natural history, the markers of progression, and the ethical consequence of detecting the disease at this asymptomatic stage. This article is aimed at addressing all the different issues by providing for each of them an updated review of the literature and evidence, with practical recommendations.

Published
2016

2. Bayesian workflow for the investigation of hierarchical classification models from tau-PET and structural MRI data across the Alzheimer's disease spectrum.

Author

Belasso, Clyde J., Zhengchen Cai, Bezgin, Gleb, Pascoal, Tharick, Stevenson, Jenna, Rahmouni, Nesrine, Tissot, Cécile, Lussier, Firoza, Rosa-Neto, Pedro, Soucy, Jean-Paul, Rivaz, Hassan, and Benali, Habib

Subjects
BRAIN physiology, ALZHEIMER'S disease diagnosis, DISEASE progression, TAU proteins, MAGNETIC resonance imaging, PSYCHOLOGICAL tests, POSITRON emission tomography, RESEARCH funding, STATISTICAL models, PROBABILITY theory
Abstract

Background: Alzheimer's disease (AD) diagnosis in its early stages remains difficult with current diagnostic approaches. Though tau neurofibrillary tangles (NFTs) generally follow the stereotypical pattern described by the Braak staging scheme, the network degeneration hypothesis (NDH) has suggested that NFTs spread selectively along functional networks of the brain. To evaluate this, we implemented a Bayesian workflow to develop hierarchical multinomial logistic regression models with increasing levels of complexity of the brain from tau-PET and structural MRI data to investigate whether it is beneficial to incorporate network-level information into an ROI-based predictive model for the presence/ absence of AD. Methods: This study included data from the Translational Biomarkers in Aging and Dementia (TRIAD) longitudinal cohort from McGill University's Research Centre for Studies in Aging (MCSA). Baseline and 1year follow-up structural MRI and [18F]MK-6240 tau-PET scans were acquired for 72 cognitive normal (CN), 23 mild cognitive impairment (MCI), and 18 Alzheimer's disease dementia subjects. We constructed the four following hierarchical Bayesian models in order of increasing complexity: (Model 1) a complete-pooling model with observations, (Model 2) a partial-pooling model with observations clustered within ROIs, (Model 3) a partial-pooling model with observations clustered within functional networks, and (Model 4) a partialpooling model with observations clustered within ROIs that are also clustered within functional brain networks. We then investigated which of the models had better predictive performance given tau-PET or structural MRI data as an input, in the form of a relative annualized rate of change. Results: The Bayesian leave-one-out cross-validation (LOO-CV) estimate of the expected log pointwise predictive density (ELPD) results indicated that models 3 and 4 were substantially better than other models for both tau-PET and structural MRI inputs. For tau-PET data, model 3 was slightly better than 4 with an absolute difference in ELPD of 3.10 ± 1.30. For structural MRI data, model 4 was considerably better than other models with an absolute difference in ELPD of 29.83 ± 7.55 relative to model 3, the second-best model. Conclusion: Our results suggest that representing the data generating process in terms of a hierarchical model that encompasses both ROI-level and network-level heterogeneity leads to better predictive ability for both tau-PET and structural MRI inputs over all other model iterations. [ABSTRACT FROM AUTHOR]

Published
2023
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3. Biomarker-guided clustering of Alzheimer's disease clinical syndromes

Author

Toschi, Nicola, Lista, Simone, Lamari, Foudil, Genthon, Remy, Habert, Marie-Odile, Dubois, Bruno, Floris, Roberto, Garaci, Francesco, Vergallo, Andrea, Hampel, Harald, group, INSIGHT-preAD study, Initiative, Alzheimer Precision Medicine, Baldacci, Filippo, Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Boukerrou, Nadia, Cavedo, Enrica, Chiesa, Patrizia, Colliot, Olivier, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Houot, Marion, Kas, Aurélie, Levy, Marcel, Zetterberg, Henrik, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Blennow, Kaj, Surtee, Mohmed, Thiebaut de Schotten, Michel, Younsi, Nadjia, Kilimann, Ingo, Teipel, Stefan J, Melo Dos Santos, Antonio, Alzheimer Precision Medicine [CHU Pitié-Salpétriêre] (GRC 21 AMP), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'Imagerie Biomédicale (LIB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), CCSD, Accord Elsevier, Università degli Studi di Roma Tor Vergata [Roma], Athinoula A. Martinos Center for Biomedical Imaging, Harvard Medical School [Boston] (HMS)-Massachusetts General Hospital [Boston], Alzheimer Precision Medicine [CHU Pitié-Salpétriêre] (GRC 21 APM), Institut du Cerveau = Paris Brain Institute (ICM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut de la Mémoire et de la Maladie d'Alzheimer [CHU Pitié-Salpétriêre] (IM2A), University of Pisa - Università di Pisa, University of Gothenburg (GU), University of Rostock, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre pour l'Acquisition et le Traitement des Images (CATI), Eisai, and Hovagim Bakardjian, Habib Benali, Hugo Bertin, Joel Bonheur, Laurie Boukadida, Nadia Boukerrou, Enrica Cavedo, Patrizia Chiesa, Olivier Colliot, Bruno Dubois, Marion Dubois, Stéphane Epelbaum, Geoffroy Gagliardi, Remy Genthon, Marie-Odile Habert, Harald Hampel, Marion Houot, Aurélie Kas, Foudil Lamari, Marcel Levy, Simone Lista, Christiane Metzinger, Fanny Mochel, Francis Nyasse, Catherine Poisson, Marie-Claude Potier, Marie Revillon, Antonio Santos, Katia Santos Andrade, Marine Sole, Mohmed Surtee, Michel Thiebaut de Schotten, Andrea Vergallo, Nadjia Younsi

Subjects
Male, 0301 basic medicine, Oncology, Aging, [SDV]Life Sciences [q-bio], cerebrospinal fluid [Amyloid beta-Peptides], Disease, 0302 clinical medicine, Risk Factors, General Neuroscience, Precision medicine, diagnosis [Alzheimer Disease], Alzheimer's disease, Middle Aged, Pathophysiology, 3. Good health, [SDV] Life Sciences [q-bio], cerebrospinal fluid [Alzheimer Disease], cerebrospinal fluid [Cognitive Dysfunction], cerebrospinal fluid [Biomarkers], Biomarker (medicine), Female, Biomarker-guided categorization, Clustering, medicine.medical_specialty, tau Proteins, Neuropathology, 03 medical and health sciences, Settore MED/36 - Diagnostica per Immagini e Radioterapia, Alzheimer Disease, Internal medicine, medicine, Humans, Dementia, Cognitive Dysfunction, ddc:610, cerebrospinal fluid [Peptide Fragments], Cluster analysis, Aged, Amyloid beta-Peptides, business.industry, medicine.disease, Settore FIS/07 - Fisica Applicata(Beni Culturali, Ambientali, Biol.e Medicin), Peptide Fragments, 030104 developmental biology, diagnosis [Cognitive Dysfunction], cerebrospinal fluid [tau Proteins], Spatial clustering, Neurology (clinical), Geriatrics and Gerontology, business, Biomarkers, 030217 neurology & neurosurgery, Developmental Biology
Abstract

International audience; Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria. We characterized the heterogeneous "construct" of AD through a cerebrospinal fluid biomarker-guided stratification approach. We analyzed 5 validated pathophysiological cerebrospinal fluid biomarkers (Aβ1-42, t-tau, p-tau181, NFL, YKL-40) in 113 participants (healthy controls [N = 20], subjective memory complainers [N = 36], mild cognitive impairment [N = 20], and AD dementia [N = 37], age: 66.7 ± 10.4, 70.4 ± 7.7, 71.7 ± 8.4, 76.2 ± 3.5 years [mean ± SD], respectively) using Density-Based Spatial Clustering of Applications with Noise, which does not require a priori determination of the number of clusters. We found 5 distinct clusters (sizes: N = 38, 16, 24, 14, and 21) whose composition was independent of phenotypical groups. Two clusters showed biomarker profiles linked to neurodegenerative processes not associated with classical AD-related pathophysiology. One cluster was characterized by the neuroinflammation biomarker YKL-40. Combining nonlinear data aggregation with informative biomarkers can generate novel patient strata which are representative of cellular/molecular pathophysiology and may aid in predicting disease evolution and mechanistic drug response.

Published
2019

4. Subjective cognitive decline and rates of incident Alzheimer's disease and non–Alzheimer's disease dementia

Author

Slot, Rosalinde E R, Sikkes, Sietske A M, Lista, Simone, Luck, Tobias, Maruff, Paul, Molinuevo, José Luis, Kornhuber, Johannes, Reisberg, Barry, Riedel-Heller, Steffi G, Risacher, Shannon L, Roehr, Susanne, Sachdev, Perminder S, Berkhof, Johannes, Scarmeas, Nikolaos, Scheltens, Philip, Shulman, Melanie B, Saykin, Andrew J, Verfaillie, Sander C J, Visser, Pieter Jelle, Vos, Stephanie J B, Wagner, Michael, Wolfsgruber, Steffen, Jessen, Frank, Brodaty, Henry, Initiative, Alzheimer's Disease Neuroimaging, group, DESCRIPA working, group, INSIGHT-preAD study, group, SCD-I working, van der Flier, Wiesje M, Boada, Mercè, de Deyn, Peter Paul, Jones, Roy, Frisoni, Giovanni, Spiru, Luiza, Buckley, Rachel, Nobili, Flavio, Freund-Levi, Yvonne, Soininen, Hilkka, Verhey, Frans, Wallin, Åsa K, Touchon, Jacques, Rikkert, Marcel Olde, Rigaud, Anne-Sophie, Bullock, Roger, Tsolaki, Magda, Cavedo, Enrica, Vellas, Bruno, Wilcock, Gordon, Hampel, Harald, Froelich, Lutz, Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Boukerrou, Nadia, Dardiotis, Efthimios, Chiesa, Patrizia, Colliot, Olivier, Dubois, Bruno, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Habert, Marie-Odile, Guillo-Benarous, Francoise, Houot, Marion, Kas, Aurélie, Lamari, Foudil, Levy, Marcel, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Surtee, Mohmed, Thiebaud de Schotten, Michel, Vergallo, Andrea, Younsi, Nadjia, Kochan, Nicole A, Psychiatrie & Neuropsychologie, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, DESCRIPA working group, INSIGHT-preAD study group, SCD-I working group, Neurology, Amsterdam Neuroscience - Neurodegeneration, Epidemiology and Data Science, APH - Methodology, APH - Personalized Medicine, and Clinical Neuropsychology

Subjects
0301 basic medicine, Male, NATIONAL INSTITUTE, Pediatrics, epidemiology [Cognitive Dysfunction], Epidemiology, Dementia incidence, Preclinical Alzheimer's disease, Vascular dementia, Cohort Studies, 0302 clinical medicine, RECRUITMENT METHODS, Risk Factors, Cognitive decline, Aged, 80 and over, Health Policy, Incidence, Hazard ratio, Middle Aged, Alzheimer's disease, IMPAIRMENT, 3. Good health, Psychiatry and Mental health, Disease Progression, Female, psychology [Cognitive Dysfunction], ASSOCIATION WORKGROUPS, Alzheimer’s disease, Frontotemporal dementia, Alzheimer's Disease Neuroimaging Initiative, MAJOR SUBTYPES, medicine.medical_specialty, psychology [Dementia], epidemiology [Dementia], Dementia Lewy bodies, Article, APOLIPOPROTEIN-E, 03 medical and health sciences, Cellular and Molecular Neuroscience, Diagnostic Self Evaluation, Developmental Neuroscience, SDG 3 - Good Health and Well-being, BASE-LINE CHARACTERISTICS, Subjective cognitive decline, Neurology (clinical), Geriatrics and Gerontology, Psychiatry and Mental Health, medicine, Dementia, Humans, Cognitive Dysfunction, ddc:610, OLDER-ADULTS, Preclinical Alzheimer’s disease, Aged, Proportional hazards model, business.industry, Memory clinic, medicine.disease, Self Concept, 030104 developmental biology, DIAGNOSTIC GUIDELINES, Human medicine, business, MEMORY COMPLAINTS, 030217 neurology & neurosurgery
Abstract

Introduction: In this multicenter study on subjective cognitive decline (SCD) in community-based and memory clinic settings, we assessed the (1) incidence of Alzheimer's disease (AD) and non-AD dementia and (2) determinants of progression to dementia.Methods: Eleven cohorts provided 2978 participants with SCD and 1391 controls. We estimated dementia incidence and identified risk factors using Cox proportional hazards models.Results: In SCD, incidence of dementia was 17.7 (95% Poisson confidence interval 15.2-20.3)/1000 person-years (AD: 11.5 [9.6-13.7], non-AD: 6.1 [4.7-7.7]), compared with 14.2 (11.3-17.6) in controls (AD: 10.1 [7.7-13.0], non-AD: 4.1 [2.6-6.0]). The risk of dementia was strongly increased in SCD in a memory clinic setting but less so in a community-based setting. In addition, higher age (hazard ratio 1.1 [95% confidence interval 1.1-1.1]), lower Mini-Mental State Examination (0.7 [0.66-0.8]), and apolipoprotein E epsilon 4 (1.8 [1.3-2.5]) increased the risk of dementia.Discussion: SCD can precede both AD and non-AD dementia. Despite their younger age, individuals with SCD in a memory clinic setting have a higher risk of dementia than those in community-based cohorts. (C) 2018 The Authors. Published by Elsevier Inc.

Published
2019

5. MiRNA-15b and miRNA-125b are associated with regional Aβ-PET and FDG-PET uptake in cognitively normal individuals with subjective memory complaints

Author

Vergallo, Andrea, Lista, Simone, group, INSIGHT-preAD study, Lucía, Alejandro, Mango, Dalila, Mapstone, Mark, Neri, Christian, Nisticò, Robert, O'Bryant, Sid E, Palermo, Giovanni, Perry, George, Ritchie, Craig, Rossi, Simone, Initiative, Alzheimer Precision Medicine, Saidi, Amira, Santarnecchi, Emiliano, Schneider, Lon S, Sporns, Olaf, Toschi, Nicola, Valenzuela, Pedro L, Vellas, Bruno, Verdooner, Steven R, Villain, Nicolas, Giudici, Kelly Virecoulon, Bakardjian, Hovagim, Watling, Mark, Welikovitch, Lindsay A, Woodcock, Janet, Younesi, Erfan, Zugaza, José L, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Boukerrou, Nadia, Cavedo, Enrica, Chiesa, Patrizia, Zhao, Yuhai, Colliot, Olivier, Dubois, Bruno, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Habert, Marie-Odile, Hampel, Harald, Houot, Marion, Kas, Aurélie, Lemercier, Pablo, Lamari, Foudil, Levy, Marcel, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Santos, Antonio, Teipel, Stefan J, Andrade, Katia Santos, Sole, Marine, Surtee, Mohmed, de Schotten, Michel Thiebaut, Younsi, Nadjia, Afshar, Mohammad, Aguilar, Lisi Flores, Akman-Anderson, Leyla, Arenas, Joaquín, Ávila, Jesús, Babiloni, Claudio, Baldacci, Filippo, Batrla, Richard, Benda, Norbert, Black, Keith L, Bokde, Arun L W, Bonuccelli, Ubaldo, Broich, Karl, Cacciola, Francesco, Caraci, Filippo, Caruso, Giuseppe, Castrillo, Juan, Ceravolo, Roberto, Chiesa, Patrizia A, Corbo, Massimo, Corvol, Jean-Christophe, Cuello, Augusto Claudio, Cummings, Jeffrey L, Depypere, Herman, Duggento, Andrea, Emanuele, Enzo, Escott-Price, Valentina, Federoff, Howard, Ferretti, Maria Teresa, Fiandaca, Massimo, Frank, Richard A, Garaci, Francesco, Lukiw, Walter J, Geerts, Hugo, Giacobini, Ezio, Giorgi, Filippo S, Goetzl, Edward J, Graziani, Manuela, Haberkamp, Marion, Hänisch, Britta, Herholz, Karl, Hernandez, Felix, Imbimbo, Bruno P, Kapogiannis, Dimitrios, Karran, Eric, Kiddle, Steven J, Kim, Seung H, Koronyo, Yosef, Koronyo-Hamaoui, Maya, Langevin, Todd, Lehéricy, Stéphane, Llavero, Francisco, Lorenceau, Jean, Ministre de l'Enseignement Supérieur, de la Recherche et de l'Innovation (France), Sorbonne Université, AXA Research Fund, Fondation partenariale, Fondation pour la Recherche sur Alzheimer, Investissement d’Avenir French program, Vergallo, Andrea [0000-0002-0208-6384], Apollo - University of Cambridge Repository, Alzheimer Precision Medicine [CHU Pitié-Salpétriêre] (GRC 21 AMP), CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut de la Mémoire et de la Maladie d'Alzheimer [Paris] (IM2A), Sorbonne Université (SU), Service de Neurologie [CHU Pitié-Salpêtrière], IFR70-CHU Pitié-Salpêtrière [AP-HP], Louisiana State University (LSU), University of Rostock, Laboratoire d'Imagerie Biomédicale (LIB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), CATI Multicenter Neuroimaging Platform (CATI), Service de médecine nucléaire [CHU Pitié-Salpétrière], Observatoire Midi-Pyrénées (OMP), Météo France-Centre National d'Études Spatiales [Toulouse] (CNES)-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD), Department of Psychiatry, Psychosomatic Medicine and Psychotherapy [Goethe Universität], Goethe-Universität Frankfurt am Main, HAL-SU, Gestionnaire, Alzheimer Precision Medicine [CHU Pitié-Salpétriêre] (GRC 21 APM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut du Cerveau = Paris Brain Institute (ICM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut de la Mémoire et de la Maladie d'Alzheimer [CHU Pitié-Salpétriêre] (IM2A), Service de Médecine nucléaire [CHU Pitié-Salpétrière], Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut national des sciences de l'Univers (INSU - CNRS)-Centre National d'Études Spatiales [Toulouse] (CNES)-Centre National de la Recherche Scientifique (CNRS)-Météo-France, Groupe de recherche clinique Alzheimer Precision Medicine (GRC 21 - APM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Laboratoire d'Imagerie Biomédicale [Paris] (LIB), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut national des sciences de l'Univers (INSU - CNRS)-Centre National d'Études Spatiales [Toulouse] (CNES)-Centre National de la Recherche Scientifique (CNRS)-Météo-France, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Service de neurologie 1 [CHU Pitié-Salpétrière], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)

Subjects
Apolipoprotein E, Aging, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Disease, miRNAs plasma concentrations, Alzheimer's Disease, amyloid-β (Aβ)-positron emission tomography (Aβ-PET), Prognostic markers, 0302 clinical medicine, Medicine, Psychology, Aetiology, education.field_of_study, MicroARNs, Settore FIS/07, amyloid, Brain, Pathophysiology, ALZHEIMERS-DISEASE, Psychiatry and Mental health, Alzheimer's disease (AD), Public Health and Health Services, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], MiRNA, medicine.medical_specialty, 18F-fluorodeoxyglucose-PET (18F-FDG-PET), BIOMARKERS, Neurociencias, Clinical Sciences, Molecular neuroscience, Predictive markers, Article, VESICLES, lcsh:RC321-571, 03 medical and health sciences, Memory, Clinical Research, Alzheimer Disease, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], microRNA, Genetics, Humans, education, Biological Psychiatry, Prevention, Memory, MiRNA, Alzheimer, biological markers, amyloid, 030104 developmental biology, Endocrinology, Cross-Sectional Studies, Positron-Emission Tomography, CELLS, Dementia, diagnostic imaging [Alzheimer Disease], INSIGHT-preAD study group, 030217 neurology & neurosurgery, [SDV.NEU.SC] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences, 0301 basic medicine, genetics [Alzheimer Disease], Pilot Projects, Neurodegenerative, Medicine and Health Sciences, 2.1 Biological and endogenous factors, genetics [MicroRNAs], MIR-125B, screening and diagnosis, PLASMA, [SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences, Detection, Real-time polymerase chain reaction, Neurological, medicine.symptom, biological markers, Biotechnology, EXPRESSION, Population, metabolism [Amyloid beta-Peptides], Asymptomatic, Salud mental, Cellular and Molecular Neuroscience, ADULT, Fluorodeoxyglucose F18, Internal medicine, Acquired Cognitive Impairment, ddc:610, Allele, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, diagnostic imaging [Brain], Psiquiatría, Amyloid beta-Peptides, Enfermedad de alzheimer, business.industry, [SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Neurosciences, Alzheimer Precision Medicine Initiative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Brain Disorders, 4.1 Discovery and preclinical testing of markers and technologies, MicroRNAs, metabolism [Brain], Alzheimer, business, Psychiatric disorders
Abstract

There is substantial experimental evidence for dysregulation of several microRNA (miRNA) expression levels in Alzheimer’s disease (AD). MiRNAs modulate critical brain intracellular signaling pathways and are associated with AD core pathophysiological mechanisms. First, we conducted a real-time quantitative PCR-based pilot study to identify a set of brain-enriched miRNAs in a monocentric cohort of cognitively normal individuals with subjective memory complaints, a condition associated with increased risk of AD. Second, we investigated the impact of age, sex, and the Apolipoprotein E ε4 (APOE ε4) allele, on the identified miRNA plasma concentrations. In addition, we explored the cross-sectional and longitudinal association of the miRNAs plasma concentrations with regional brain metabolic uptake using amyloid-β (Aβ)-positron emission tomography (Aβ-PET) and F-fluorodeoxyglucose-PET (F-FDG-PET). We identified a set of six brain-enriched miRNAs—miRNA-125b, miRNA-146a, miRNA-15b, miRNA-148a, miRNA-26b, and miRNA-100. Age, sex, and APOE ε4 allele were not associated with individual miRNA abundance. MiRNA-15b concentrations were significantly lower in the Aβ-PET-positive compared to Aβ-PET-negative individuals. Furthermore, we found a positive effect of the miRNA-15b*time interaction on regional metabolic F-FDG-PET uptake in the left hippocampus. Plasma miRNA-125b concentrations, as well as the miRNA-125b*time interaction (over a 2-year follow-up), were negatively associated with regional Aβ-PET standard uptake value ratio in the right anterior cingulate cortex. At baseline, we found a significantly negative association between plasma miRNA-125b concentrations and F-FDG-PET uptake in specific brain regions. In an asymptomatic at-risk population for AD, we show significant associations between plasma concentrations of miRNA-125b and miRNA-15b with core neuroimaging biomarkers of AD pathophysiology. Our results, coupled with existing experimental evidence, suggest a potential protective anti-Aβ effect of miRNA-15b and a biological link between miRNA-125b and Aβ-independent neurotoxic pathways., “Investissement d’Avenir” (ANR-10-AIHU-06) French program. The study was promoted in collaboration with the “CHU de Bordeaux” (coordination CIC EC7), the promoter of Memento cohort, funded by the Foundation Plan-Alzheimer. The study was further supported by AVID/Lilly. CATI is a French neuroimaging platform funded by the French Plan Alzheimer (available at http://cati-neuroimaging.com). A.V. is an employee of Eisai Inc. This work has been performed during his previous position at Sorbonne University, Paris, France. H.H. is an employee of Eisai Inc. This work has been performed during his previous position at Sorbonne University, Paris, France. At Sorbonne University he was supported by the AXA Research Fund, the “Fondation partenariale Sorbonne Université” and the “Fondation pour la Recherche sur Alzheimer

Published
2021

8. Plasma tau correlates with basal forebrain atrophy rates in people at risk for alzheimer disease

Author

Cavedo, Enrica, Lista, Simone, Dubois, Bruno, Mapstone, Mark, Neri, Christian, Nistico, Robert, O'Bryant, Sid E., Palermo, Giovanni, Perry, George, Ritchie, Craig, Rossi, Simone, Saidi, Amira, Santarnecchi, Emilian, Hampel, Harald, Schneider, Lon S., Sporns, Olaf, Toschi, Nicola, Verdooner, Steven R., Vergallo, Andrea, Villain, Nicolas, Welikovitch, Lindsay A., Woodcock, Janet, Younesi, Erfan, Group, INSIGHT-preAD Study, Alzheimer Precision Medicine Initiative, Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Houot, Marion, Chiesa, Patrizia, Colliot, Olivier, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Habert, Marie-Odile, Hampe, Harald, Kas, Auréli, Lamari, Foudil, Levy, Marcel, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Potier, Marie-Claude, Revillon, Marie, Grothe, Michel J, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Thiebaud de Schotten, Michel, Andrea, Vergallo, Nadjia, Yonsi, Afshar, Mohammad, Aguilar, Lisi Flores, Akman-Anderson, Leyla, Teipel, Stefan, Arenas, Joaquín, Avila, Jesus, Babiloni, Claudio, Baldacci, Filippo, Batrla, Richard, Benda, Norbert, Black, Keith L., Bokde, Arun L. W., Bonuccelli, Ubaldo, Broich, Karl, Zetterberg, Henrik, Caccilola, Francesco, Caraci, Filippo, Castrillo, Juan, Ceravolo, Roberto, Chiesa, Patrizia A., Corvol, Jean-Christophe, Cuello, Augusto Claudio, Cummings, Jeffrey L., Depypere, Herman, Blennow, Kaj, Duggent, Andrea, Emanuele, Enzo, Escott-Price, Valentina, Federoff, Howard, Ferretti, Maria Teresa, Fiandaca, Massimo, Frank, Richard A., Garaci, Francesco, Geerts, Hugo, Giorgi, Filippo S., Goetzl, Edward J., Graziani, Manuela, Haberkamp, Marion, Herholz, Karl, Hernandez, Felix, Kapogiannis, Dimitrios, Karran, Eric, Potier, Marie C, Kidddle, Stephen J, Kim, Seung H., Koronyo, Yosef, Koronyo-Hamaoui, Maya, Langevin, Todd, Lehericy, Stéphane, Lucia, Alejandro, Lorenceau, Jean, and Mango, Dalila

Subjects
0301 basic medicine, Apolipoprotein E, Male, blood [Neurofilament Proteins], Cohort Studies, pathology [Alzheimer Disease], 0302 clinical medicine, pathology [Prosencephalon], Neurofilament Proteins, blood [Amyloid beta-Peptides], Basal forebrain, pathology [Parasympathetic Nervous System], Magnetic Resonance Imaging, Predictive value of tests, Cohort, Female, Alzheimer's disease, Cohort study, blood [tau Proteins], medicine.medical_specialty, tau Proteins, 03 medical and health sciences, aged, alzheimer disease, amyloid beta-peptides, apolipoproteins e, atrophy, biomarkers, cohort studies, female, humans, magnetic resonance imaging, male, neurofilament proteins, parasympathetic nervous system, positron-emission tomography, predictive value of tests, prosencephalon, tau proteins, Atrophy, blood [Alzheimer Disease], Apolipoproteins E, Prosencephalon, Alzheimer Disease, Parasympathetic Nervous System, Predictive Value of Tests, Internal medicine, medicine, Dementia, Humans, ddc:610, Aged, Amyloid beta-Peptides, business.industry, diagnostic imaging [Prosencephalon], medicine.disease, 030104 developmental biology, Endocrinology, Positron-Emission Tomography, genetics [Apolipoproteins E], Neurology (clinical), business, diagnostic imaging [Alzheimer Disease], 030217 neurology & neurosurgery, Biomarkers
Abstract

ObjectiveTo investigate whether baseline concentrations of plasma total tau (t-tau) and neurofilament light (NfL) chain proteins are associated with annual percent change (APC) of the basal forebrain cholinergic system (BFCS) in cognitively intact older adults at risk for Alzheimer disease (AD).MethodsThis was a large-scale study of 276 cognitively intact older adults from the monocentric INSIGHT-preAD (Investigation of Alzheimer's Predictors in Subjective Memory Complainers) cohort. Participants underwent baseline assessment of plasma t-tau and NfL concentrations as well as baseline and 24-month follow-up MRI scans. Linear models with and without influential observations (calculated using the Cook distance) were carried out to investigate the effect of plasma NfL and t-tau concentrations, and their interaction effect with β-amyloid status and APOE genotype, on the APC of the whole BFCS and its anterior (Ch1/2) and posterior (Ch4) subdivisions separately.ResultsHigher plasma t-tau concentrations at baseline were associated with higher BFCS rate of atrophy (model without influencers: n = 251, F value = 4.6815; p value = 0.031). Subregional analyses showed similar results for both the APC of the Ch1/2 (model without influencers: n = 256, F value = 3.9535, p corrected = 0.047) and Ch4 BFCS sectors (model without influencers: n = 253, F value = 4.9090, p corrected = 0.047). Baseline NfL, β-amyloid load, and APOE ε4 carrier status did not affect APC of the BFCS.ConclusionIncreased concentrations of baseline plasma t-tau may predict in vivo structural BFCS atrophy progression in older adults at risk for AD, independently of β-amyloid status and APOE genotype.

Published
2020

9. Sex differences in functional and molecular neuroimaging biomarkers of Alzheimer's disease in cognitively normal older adults with subjective memory complaints

Author

Cavedo, Enrica, Chiesa, Patrizia A., Houot, Marion, Ferretti, Maria Teresa, Grothe, Michel J., Teipel, Stefan J., Lista, Simone, Habert, Marie-Odile, Potier, Marie-Claude, Dubois, Bruno, Hampel, Harald, Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, Boukerrou, Nadia, Chiesa, Patrizia, Colliot, Olivier, Dubois, Marion, Epelbaum, Stéphane, Gagliardi, Geoffroy, Genthon, Remy, Kas, Aurélie, Lamari, Foudil, Levy, Marcel, Metzinger, Christiane, Mochel, Fanny, Nyasse, Francis, Poisson, Catherine, Revillon, Marie, Santos, Antonio, Andrade, Katia Santos, Sole, Marine, Surtee, Mohmed, de Schotten, Michel Thiebaud, Vergallo, Andrea, Younsi, Nadjia, Aguilar, Lisi Flores, Babiloni, Claudio, Baldacci, Filippo, Benda, Norbert, Black, Keith L., Bokde, Arun L. W., Bonuccelli, Ubaldo, Broich, Karl, Bun, René S., Cacciola, Francesco, Castrillo, Juan, Ceravolo, Roberto, Coman, Cristina-Maria, Corvol, Jean-Christophe, Cuello, Augusto Claudio, Cummings, Jeffrey L., Depypere, Herman, Duggento, Andrea, Durrleman, Stanley, Escott-Price, Valentina, Federoff, Howard, Fiandaca, Massimo, Frank, Richard A., Garaci, Francesco, George, Nathalie, Giorgi, Filippo S., Graziani, Manuela, Haberkamp, Marion, Herholz, Karl, Karran, Eric, Kim, Seung H., Koronyo, Yosef, Koronyo-Hamaoui, Maya, Langevin, Todd, Lehéricy, Stéphane, Lorenceau, Jean, Mapstone, Mark, Neri, Christian, Nisticò, Robert, Nyasse-Messene, Francis, O'Bryant, Sid E., Perry, George, Ritchie, Craig, Rojkova, Katrine, Rossi, Simone, Saidi, Amira, Santarnecchi, Emiliano, Schneider, Lon S., Sporns, Olaf, Toschi, Nicola, Verdooner, Steven R., Villain, Nicolas, Welikovitch, Lindsay A., Woodcock, Janet, and Younesi, Erfan

Subjects
Male, 0301 basic medicine, Apolipoprotein E, Oncology, Aging, aging, Alzheimer's disease, amyloid, APOE, basal forebrain, cognitively intact older individuals, cortical thickness, FDG-PET, hippocampus, metabolism, sex, epidemiology, health policy, developmental neuroscience, neurology (clinical), geriatrics and gerontology, cellular and molecular neuroscience, psychiatry and mental health, Epidemiology, Cognitively intact older individuals, Precuneus, Hippocampus, genetics [Alzheimer Disease], physiopathology [Brain], Cohort Studies, 0302 clinical medicine, genetics [Memory Disorders], Risk Factors, Neural Pathways, Medicine, Aged, 80 and over, Sex Characteristics, Health Policy, Settore FIS/07, Neurodegeneration, Brain, Human brain, Magnetic Resonance Imaging, diagnostic imaging [Neural Pathways], Psychiatry and Mental health, metabolism [Glucose], medicine.anatomical_structure, Female, Sex, Amyloid, medicine.medical_specialty, Rest, diagnostic imaging [Memory Disorders], physiopathology [Alzheimer Disease], Cortical thickness, Basal forebrain, Diagnostic Self Evaluation, 03 medical and health sciences, Cellular and Molecular Neuroscience, Apolipoproteins E, Sex Factors, Developmental Neuroscience, Alzheimer Disease, Internal medicine, physiopathology [Memory Disorders], Humans, ddc:610, diagnostic imaging [Brain], Metabolism, Anterior cingulate cortex, metabolism [Amyloid], Aged, Memory Disorders, Resting state fMRI, business.industry, physiopathology [Neural Pathways], medicine.disease, Glucose, 030104 developmental biology, psychology [Memory Disorders], Positron-Emission Tomography, Posterior cingulate, genetics [Apolipoproteins E], Neurology (clinical), Geriatrics and Gerontology, business, diagnostic imaging [Alzheimer Disease], 030217 neurology & neurosurgery
Abstract

Observational multimodal neuroimaging studies indicate sex differences in Alzheimer's disease pathophysiological markers.Positron emission tomography brain amyloid load, neurodegeneration (hippocampus and basal forebrain volumes adjusted to total intracranial volume, cortical thickness, and 2-deoxy-2-[fluorine-18]fluoro-D-glucose-positron emission tomography metabolism), and brain resting-state functional connectivity were analyzed in 318 cognitively intact older adults from the INSIGHT-preAD cohort (female n = 201, male n = 117). A linear mixed-effects model was performed to investigate sex effects and sex∗apolipoprotein E genotype interaction on each marker as well as sex∗amyloid group interaction for non-amyloid markers.Men compared with women showed higher anterior cingulate cortex amyloid load (P = .009), glucose hypometabolism in the precuneus (P = .027), posterior cingulate (P .001) and inferior parietal (P = .043) cortices, and lower resting-state functional connectivity in the default mode network (P = .024). No brain volumetric markers showed differences between men and women. Sex∗apolipoprotein E genotype and sex∗amyloid status interactions were not significant.Our findings suggest that cognitively intact older men compared with women have higher resilience to pathophysiological processes of Alzheimer's disease.

Published
2018

10. Preclinical Alzheimer's disease: Definition, natural history, and diagnostic criteria

Author

Proceedings of the Meeting of the International Working Group (IWG) and the American Alzheimer's Association on 'The Preclinical State of AD', Dubois, Bruno, Hampel, Harald, Feldman, Howard H, Scheltens, Philip, Aisen, Paul, Andrieu, Sandrine, Bakardjian, Hovagim, Benali, Habib, Bertram, Lars, Blennow, Kaj, Broich, Karl, Cavedo, Enrica, Crutch, Sebastian, Dartigues, Jean-François, Duyckaerts, Charles, Epelbaum, Stéphane, Frisoni, Giovanni B, Gauthier, Serge, Genthon, Remy, Gouw, Alida A, Habert, Marie-Odile, Holtzman, David M, Kivipelto, Miia, Lista, Simone, Molinuevo, José-Luis, O'Bryant, Sid E, Rabinovici, Gil D, Rowe, Christopher, Salloway, Stephen, Schneider, Lon S, Sperling, Reisa, Teichmann, Marc, Carrillo, Maria C, Cummings, Jeffrey, and Jack, Cliff R

Subjects
Aging, Diagnostic criteria, Clinical Sciences, Neurodegenerative, Alzheimer's Disease, Pathophysiology, Blood biomarkers, Alzheimer Disease, Genetics, Acquired Cognitive Impairment, Animals, Humans, Tau PET, Washington DC, CSF biomarkers, USA, Human Genome, Neurosciences, Brain, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Proceedings of the Meeting of the International Working Group (IWG) and the American Alzheimer's Association on “The Preclinical State of AD”, Preclinical, July 23, Asymptomatic, Brain Disorders, Amyloid PET, Geriatrics, Neurological, Disease Progression, Dementia, Biomarkers, MRI
Abstract

During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum. Thanks to evolving biomarker research and substantial discoveries, it is now possible to identify the disease even at the preclinical stage before the occurrence of the first clinical symptoms. This preclinical stage of AD has become a major research focus as the field postulates that early intervention may offer the best chance of therapeutic success. To date, very little evidence is established on this "silent" stage of the disease. A clarification is needed about the definitions and lexicon, the limits, the natural history, the markers of progression, and the ethical consequence of detecting the disease at this asymptomatic stage. This article is aimed at addressing all the different issues by providing for each of them an updated review of the literature and evidence, with practical recommendations.

Published
2016

11. Extended fractional-polynomial generalizations of diffusion and Fisher–KPP equations on directed networks.

Author

Rahimabadi, Arsalan and Benali, Habib

Subjects
*REACTION-diffusion equations, *HEAT equation, *DIRECTED graphs, *LAPLACIAN operator, *INVARIANT sets, *ALZHEIMER'S disease, *UNDIRECTED graphs
Abstract

In a variety of practical applications, there is a need to investigate diffusion or reaction–diffusion processes on complex structures, including brain networks, that can be modeled as weighted undirected and directed graphs. As an instance, the celebrated Fisher–Kolmogorov–Petrovsky–Piskunov (Fisher–KPP) reaction–diffusion equation is becoming increasingly popular for use in graph frameworks by substituting the standard graph Laplacian operator for the continuous one to study the progression of neurodegenerative diseases such as Alzheimer's disease (AD). In this work, we establish existence, uniqueness, and boundedness of solutions for generalized Fisher–KPP reaction–diffusion equations on undirected and directed networks with fractional polynomial (FP) terms. This type of model has possible applications for modeling spreading of diseases within neuronal fibers whose porous structure may cause particles to diffuse anomalously. In the case of pure diffusion, convergence of solutions and stability of equilibria are also analyzed. Moreover, different families of positively invariant sets for the proposed equations are derived. Finally, we conclude by investigating nonlinear diffusion on a directed one-dimensional lattice. • The extended fractional polynomial diffusion equation on digraphs is introduced. • Existence, uniqueness, and convergence of solutions are established. • The extended FP Fisher–KPP reaction–diffusion equation on digraphs is introduced. • Different families of positively invariant sets are presented. [ABSTRACT FROM AUTHOR]

Published
2023
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12. Comment on the article "Spatially-extended nucleation-aggregation-fragmentation models for the dynamics of prion-like neurodegenerative protein-spreading in the brain and its connectome 486 (2020) 110102".

Author

Rahimabadi, Arsalan and Benali, Habib

Subjects
*PRIONS, *ALZHEIMER'S disease
Abstract

Considering the reaction schemes (20) and (21) in Fornari et al. (2020) , the fragmentation terms F i (Eq. (22) in Fornari et al. (2020)) are not correct. Thus, the fragmentation terms F i (Eq. (12) in Fornari et al. (2020)) are also incorrect when the reaction schemes (10) and (11) in Fornari et al. (2020) are taken into account. Here, the correct equations will be presented. [ABSTRACT FROM AUTHOR]

Published
2022
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13. Spatial and Anatomical Regularization of SVM: A General Framework for Neuroimaging Data.

Author

Cuingnet, Rémi, Glaunès, Joan Alexis, Chupin, Marie, Benali, Habib, and Colliot, Olivier

Subjects
BRAIN imaging, FISHER discriminant analysis, LAPLACIAN matrices, GRAPH theory, MAGNETIC resonance imaging
Abstract

This paper presents a framework to introduce spatial and anatomical priors in SVM for brain image analysis based on regularization operators. A notion of proximity based on prior anatomical knowledge between the image points is defined by a graph (e.g., brain connectivity graph) or a metric (e.g., Fisher metric on statistical manifolds). A regularization operator is then defined from the graph Laplacian, in the discrete case, or from the Laplace-Beltrami operator, in the continuous case. The regularization operator is then introduced into the SVM, which exponentially penalizes high-frequency components with respect to the graph or to the metric and thus constrains the classification function to be smooth with respect to the prior. It yields a new SVM optimization problem whose kernel is a heat kernel on graphs or on manifolds. We then present different types of priors and provide efficient computations of the Gram matrix. The proposed framework is finally applied to the classification of brain Magnetic Resonance (MR) images (based on Gray Matter (GM) concentration maps and cortical thickness measures) from 137 patients with Alzheimer's Disease (AD) and 162 elderly controls. The results demonstrate that the proposed classifier generates less-noisy and consequently more interpretable feature maps with high classification performances. [ABSTRACT FROM AUTHOR]

Published
2013
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14. Age and sex impact plasma NFL and t-Tau trajectories in individuals with subjective memory complaints: a 3-year follow-up study.

Author

Baldacci, Filippo, Lista, Simone, Manca, Maria Laura, Chiesa, Patrizia A., Cavedo, Enrica, Lemercier, Pablo, Zetterberg, Henrik, Blennow, Kaj, Habert, Marie-Odile, Potier, Marie Claude, Dubois, Bruno, Vergallo, Andrea, Hampel, Harald, the INSIGHT-preAD study group, Bakardjian, Hovagim, Benali, Habib, Bertin, Hugo, Bonheur, Joel, Boukadida, Laurie, and Boukerrou, Nadia

Subjects
BIOMARKERS, ALZHEIMER'S disease, VITAMIN B12, VITAMIN deficiency, MEMORY
Abstract

Background: Plasma neurofilament light (NFL) and total Tau (t-Tau) proteins are candidate biomarkers for early stages of Alzheimer's disease (AD). The impact of biological factors on their plasma concentrations in individuals with subjective memory complaints (SMC) has been poorly explored. We longitudinally investigate the effect of sex, age, APOE ε4 allele, comorbidities, brain amyloid-β (Aβ) burden, and cognitive scores on plasma NFL and t-Tau concentrations in cognitively healthy individuals with SMC, a condition associated with AD development. Methods: Three hundred sixteen and 79 individuals, respectively, have baseline and three-time point assessments (at baseline, 1-year, and 3-year follow-up) of the two biomarkers. Plasma biomarkers were measured with an ultrasensitive assay in a mono-center cohort (INSIGHT-preAD study). Results: We show an effect of age on plasma NFL, with women having a higher increase of plasma t-Tau concentrations compared to men, over time. The APOE ε4 allele does not affect the biomarker concentrations while plasma vitamin B12 deficiency is associated with higher plasma t-Tau concentrations. Both biomarkers are correlated and increase over time. Baseline NFL is related to the rate of Aβ deposition at 2-year follow-up in the left-posterior cingulate and the inferior parietal gyri. Baseline plasma NFL and the rate of change of plasma t-Tau are inversely associated with cognitive score. Conclusion: We find that plasma NFL and t-Tau longitudinal trajectories are affected by age and female sex, respectively, in SMC individuals. Exploring the influence of biological variables on AD biomarkers is crucial for their clinical validation in blood. [ABSTRACT FROM AUTHOR]

Published
2020
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15. Cognitive and neuroimaging features and brain β-amyloidosis in individuals at risk of Alzheimer's disease (INSIGHT-preAD): a longitudinal observational study.

Author

Dubois, Bruno, Epelbaum, Stephane, Nyasse, Francis, Bakardjian, Hovagim, Gagliardi, Geoffroy, Uspenskaya, Olga, Houot, Marion, Lista, Simone, Cacciamani, Federica, Potier, Marie-Claude, Bertrand, Anne, Lamari, Foudil, Benali, Habib, Mangin, Jean-François, Colliot, Olivier, Genthon, Remy, Habert, Marie-Odile, Hampel, Harald, and INSIGHT-preAD study group

Subjects
*COGNITIVE ability, *ALZHEIMER'S disease risk factors, *COGNITIVE development, *BRAIN imaging, *DISEASE progression, *ALZHEIMER'S disease, *BRAIN, *COGNITION, *COMPARATIVE studies, *LONGITUDINAL method, *MAGNETIC resonance imaging, *NEUROPSYCHOLOGICAL tests, *RESEARCH methodology, *MEDICAL cooperation, *NEURORADIOLOGY, *PEPTIDES, *RESEARCH, *POSITRON emission tomography, *EVALUATION research, *PSYCHOLOGY, BRAIN metabolism
Abstract

Background: Improved understanding is needed of risk factors and markers of disease progression in preclinical Alzheimer's disease. We assessed associations between brain β-amyloidosis and various cognitive and neuroimaging parameters with progression of cognitive decline in individuals with preclinical Alzheimer's disease.Methods: The INSIGHT-preAD is an ongoing single-centre observational study at the Salpêtrière Hospital, Paris, France. Eligible participants were age 70-85 years with subjective memory complaints but unimpaired cognition and memory (Mini-Mental State Examination [MMSE] score ≥27, Clinical Dementia Rating score 0, and Free and Cued Selective Reminding Test [FCSRT] total recall score ≥41). We stratified participants by brain amyloid β deposition on 18F-florbetapir PET (positive or negative) at baseline. All patients underwent baseline assessments of demographic, cognitive, and psychobehavioural, characteristics, APOE ε4 allele carrier status, brain structure and function on MRI, brain glucose-metabolism on 18F-fluorodeoxyglucose (18F-FDG) PET, and event-related potentials on electroencephalograms (EEGs). Actigraphy and CSF investigations were optional. Participants were followed up with clinical, cognitive, and psychobehavioural assessments every 6 months, neuropsychological assessments, EEG, and actigraphy every 12 months, and MRI, and 18F-FDG and 18F-florbetapir PET every 24 months. We assessed associations of amyloid β deposition status with test outcomes at baseline and 24 months, and with clinical status at 30 months. Progression to prodromal Alzheimer's disease was defined as an amnestic syndrome of the hippocampal type.Findings: From May 25, 2013, to Jan 20, 2015, we enrolled 318 participants with a mean age of 76·0 years (SD 3·5). The mean baseline MMSE score was 28·67 (SD 0·96), and the mean level of education was high (score >6 [SD 2] on a scale of 1-8, where 1=infant school and 8=higher education). 88 (28%) of 318 participants showed amyloid β deposition and the remainder did not. The amyloid β subgroups did not differ for any psychobehavioural, cognitive, actigraphy, and structural and functional neuroimaging results after adjustment for age, sex, and level of education More participants positive for amyloid β deposition had the APOE ε4 allele (33 [38%] vs 29 [13%], p<0·0001). Amyloid β1-42 concentration in CSF significantly correlated with mean 18F-florbetapir uptake at baseline (r=-0·62, p<0·0001) and the ratio of amyloid β1-42 to amyloid β1-40 (r=-0·61, p<0·0001), and identified amyloid β deposition status with high accuracy (mean area under the curve values 0·89, 95% CI 0·80-0·98 and 0·84, 0·72-0·96, respectively). No difference was seen in MMSE (28·3 [SD 2·0] vs 28·9 [1·2], p=0·16) and Clinical Dementia Rating scores (0·06 [0·2] vs 0·05 [0·3]; p=0·79) at 30 months (n=274) between participants positive or negative for amyloid β. Four participants (all positive for amyloid β deposition at baseline) progressed to prodromal Alzheimer's disease. They were older than other participants positive for amyloid β deposition at baseline (mean 80·2 years [SD 4·1] vs 76·8 years [SD 3·4]) and had greater 18F-florbetapir uptake at baseline (mean standard uptake value ratio 1·46 [SD 0·16] vs 1·02 [SD 0·20]), and more were carriers of the APOE ε4 allele (three [75%] of four vs 33 [39%] of 83). They also had mild executive dysfunction at baseline (mean FCSRT free recall score 21·25 [SD 2·75] vs 29·08 [5·44] and Frontal Assessment Battery total score 13·25 [1·50] vs 16·05 [1·68]).Interpretation: Brain β-amyloidosis alone did not predict progression to prodromal Alzheimer's disease within 30 months. Longer follow-up is needed to establish whether this finding remains consistent.Funding: Institut Hospitalo-Universitaire and Institut du Cerveau et de la Moelle Epinière (IHU-A-ICM), Ministry of Research, Fondation Plan Alzheimer, Pfizer, and Avid. [ABSTRACT FROM AUTHOR]

Published
2018
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16. Characteristics of the default mode functional connectivity in normal ageing and Alzheimer's disease using resting state fMRI with a combined approach of entropy-based and graph theoretical measurements.

Author

Toussaint, Paule-Joanne, Maiz, Sofiane, Coynel, David, Doyon, Julien, Messé, Arnaud, de Souza, Leonardo Cruz, Sarazin, Marie, Perlbarg, Vincent, Habert, Marie-Odile, and Benali, Habib

Subjects
*ALZHEIMER'S disease diagnosis, *BRAIN function localization, *ENTROPY (Information theory), *AGING, *MILD cognitive impairment
Abstract

Cognitive decline in normal ageing and Alzheimer's disease (AD) emerges from functional disruption in the coordination of large-scale brain systems sustaining cognition. Integrity of these systems can be examined by correlation methods based on analysis of resting state functional magnetic resonance imaging (fMRI). Here we investigate functional connectivity within the default mode network (DMN) in normal ageing and AD using resting state fMRI. Images from young and elderly controls, and patients with AD were processed using spatial independent component analysis to identify the DMN. Functional connectivity was quantified using integration and indices derived from graph theory. Four DMN sub-systems were identified: Frontal (medial and superior), parietal (precuneus–posterior cingulate, lateral parietal), temporal (medial temporal), and hippocampal (bilateral). There was a decrease in antero-posterior interactions (lower global efficiency), but increased interactions within the frontal and parietal sub-systems (higher local clustering) in elderly compared to young controls. This decreased antero-posterior integration was more pronounced in AD patients compared to elderly controls, particularly in the precuneus–posterior cingulate region. Conjoint knowledge of integration measures and graph indices in the same data helps in the interpretation of functional connectivity results, as comprehension of one measure improves with understanding of the other. The approach allows for complete characterisation of connectivity changes and could be applied to other resting state networks and different pathologies. [ABSTRACT FROM AUTHOR]

Published
2014
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17. Resting state FDG-PET functional connectivity as an early biomarker of Alzheimer's disease using conjoint univariate and independent component analyses

Author

Toussaint, Paule-Joanne, Perlbarg, Vincent, Bellec, Pierre, Desarnaud, Serge, Lacomblez, Lucette, Doyon, Julien, Habert, Marie-Odile, and Benali, Habib

Subjects
*ALZHEIMER'S disease, *POSITRON emission tomography, *BIOMARKERS, *UNIVARIATE analysis, *COHORT analysis, *MILD cognitive impairment, *BRAIN tomography, *INDEPENDENT component analysis
Abstract

Abstract: Imaging cerebral glucose metabolism with positron emission tomography (PET) in Alzheimer''s disease (AD) has allowed for improved characterisation of this pathology. Such patterns are typically analysed using either univariate or multivariate statistical techniques. In this work we combined voxel-based group analysis and independent component analysis to extract differential characteristic patterns from PET data of glucose metabolism in a large cohort of normal elderly controls and patients with AD. The patterns were used in conjunction with a support vector machine to discriminate between subjects with mild cognitive impairment (MCI) at risk or not of converting to AD. The method was applied to baseline fluoro-deoxyglucose (FDG)-PET images of subjects from the ADNI database. Our approach achieved improved early detection and differentiation of typical versus pathological metabolic patterns in the MCI population, reaching 80% accuracy (85% sensitivity and 75% specificity) when using selected regions. The method has the potential to assist in the advance diagnosis of Alzheimer''s disease, and to identify early in the development of the disease those individuals at high risk of rapid cognitive decline who could be candidates for new therapeutic approaches. [Copyright &y& Elsevier]

Published
2012
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18. Automatic classification of patients with Alzheimer's disease from structural MRI: A comparison of ten methods using the ADNI database

Author

Cuingnet, Rémi, Gerardin, Emilie, Tessieras, Jérôme, Auzias, Guillaume, Lehéricy, Stéphane, Habert, Marie-Odile, Chupin, Marie, Benali, Habib, and Colliot, Olivier

Subjects
*BRAIN imaging, *MILD cognitive impairment, *SUPPORT vector machines, *VOXEL-based morphometry, *AUTOMATIC classification, *ALZHEIMER'S patients, *MAGNETIC resonance imaging of the brain
Abstract

Abstract: Recently, several high dimensional classification methods have been proposed to automatically discriminate between patients with Alzheimer''s disease (AD) or mild cognitive impairment (MCI) and elderly controls (CN) based on T1-weighted MRI. However, these methods were assessed on different populations, making it difficult to compare their performance. In this paper, we evaluated the performance of ten approaches (five voxel-based methods, three methods based on cortical thickness and two methods based on the hippocampus) using 509 subjects from the ADNI database. Three classification experiments were performed: CN vs AD, CN vs MCIc (MCI who had converted to AD within 18months, MCI converters — MCIc) and MCIc vs MCInc (MCI who had not converted to AD within 18months, MCI non-converters — MCInc). Data from 81 CN, 67 MCInc, 39 MCIc and 69 AD were used for training and hyperparameters optimization. The remaining independent samples of 81 CN, 67 MCInc, 37 MCIc and 68 AD were used to obtain an unbiased estimate of the performance of the methods. For AD vs CN, whole-brain methods (voxel-based or cortical thickness-based) achieved high accuracies (up to 81% sensitivity and 95% specificity). For the detection of prodromal AD (CN vs MCIc), the sensitivity was substantially lower. For the prediction of conversion, no classifier obtained significantly better results than chance. We also compared the results obtained using the DARTEL registration to that using SPM5 unified segmentation. DARTEL significantly improved six out of 20 classification experiments and led to lower results in only two cases. Overall, the use of feature selection did not improve the performance but substantially increased the computation times. [Copyright &y& Elsevier]

Published
2011
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