title: Cognitive reserve proxies relate to gray matter loss in cognitively healthy elderly with abnormal cerebrospinal fluid amyloid-β levels.
abstract: Cognitive reserve capacity may increase tolerance of neurodegenerative processes. However, its role regarding amyloid-β (Aβ42) deposition in cognitively normal subjects is not well understood. We aimed to investigate the association between areas showing Aβ42-related structural changes and cognitive reserve proxies in cognitively intact subjects showing normal or abnormal Aβ42 cerebrospinal fluid (CSF) concentrations. Thirty-three subjects (aged 55-85) underwent lumbar puncture and high resolution anatomical magnetic resonance imaging analyzed by voxel-based morphometry and cortical thickness procedures. Subjects with abnormal Aβ42 CSF levels showed significant left hippocampal atrophy and greater cortical thinning in parietal, temporal, and frontal regions (including the supramarginal and the anterior cingulate gyrus) compared to subjects with normal Aβ42 CSF levels. Using a multivariate general linear model, we investigated the relationship between these areas and cognitive reserve proxies. We found a significant relationship between decreased volume of the left hippocampus or decreased cortical thickness of the right supramarginal gyrus and higher cognitive reserve proxies only in the group with abnormal Aβ42 CSF levels. Thus, subjects with abnormal Aβ42 CSF levels (which may be at a higher risk of developing Alzheimer's disease) and with high scores on cognitive reserve proxies may be tolerating a more advanced neurodegenerative process in critical cortical and subcortical regions. The present results emphasize the relevance of evaluating cognitive reserve proxies, as well as the importance of using neuroimaging techniques for early diagnosis in individuals with higher reserve.
authors.affiliation: Departament de Psiquiatria i Psicobiologia Clínica, Universitat de Barcelona, Catalonia, Spain.
authors.forename: Eider M
authors.initials: EM
authors.lastname: Arenaza-Urquijo
authors.forename: José-Luis
authors.initials: JL
authors.lastname: Molinuevo
authors.forename: Roser
authors.initials: R
authors.lastname: Sala-Llonch
authors.forename: Cristina
authors.initials: C
authors.lastname: Solé-Padullés
authors.forename: Mircea
authors.initials: M
authors.lastname: Balasa
authors.forename: Beatriz
authors.initials: B
authors.lastname: Bosch
authors.forename: Jaume
authors.initials: J
authors.lastname: Olives
authors.forename: Anna
authors.initials: A
authors.lastname: Antonell
authors.forename: Albert
authors.initials: A
authors.lastname: Lladó
authors.forename: Raquel
authors.initials: R
authors.lastname: Sánchez-Valle
authors.forename: Lorena
authors.initials: L
authors.lastname: Rami
authors.forename: David
authors.initials: D
authors.lastname: Bartrés-Faz
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000134:cerebrospinal fluid; D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid*; D001057:Apolipoproteins E / Q000235:genetics; D001921:Brain / Q000473:pathology*; D002540:Cerebral Cortex / Q000473:pathology; D003071:Cognition / Q000502:physiology*; D058245:Cognitive Reserve / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D016014:Linear Models; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009483:Neuropsychological Tests; D016875:tau Proteins / Q000134:cerebrospinal fluid
chemical_list: D016229:Amyloid beta-Peptides; D001057:Apolipoproteins E; D016875:tau Proteins