Cognitive reserve and clinical progression in Alzheimer disease: A paradoxical relationship.
Aged
Aged, 80 and over
Alzheimer Disease
/ cerebrospinal fluid
Amyloid beta-Peptides
/ cerebrospinal fluid
Aniline Compounds
Case-Control Studies
Cognitive Dysfunction
/ cerebrospinal fluid
Cognitive Reserve
Contrast Media
Disease Progression
Ethylene Glycols
Executive Function
Female
Gray Matter
/ diagnostic imaging
Humans
Male
Memory
Middle Aged
Organ Size
Peptide Fragments
/ cerebrospinal fluid
Thiazoles
White Matter
/ diagnostic imaging
Journal
Neurology
ISSN: 1526-632X
Titre abrégé: Neurology
Pays: United States
ID NLM: 0401060
Informations de publication
Date de publication:
23 07 2019
23 07 2019
Historique:
received:
19
10
2018
accepted:
08
03
2019
pubmed:
4
7
2019
medline:
8
1
2020
entrez:
4
7
2019
Statut:
ppublish
Résumé
To investigate the relationship between cognitive reserve (CR) and clinical progression across the Alzheimer disease (AD) spectrum. We selected 839 β-amyloid (Aβ)-positive participants with normal cognition (NC, n = 175), mild cognitive impairment (MCI, n = 437), or AD dementia (n = 227) from the Alzheimer's Disease Neuroimaging Initiative (ADNI). CR was quantified using standardized residuals (W scores) from a (covariate-adjusted) linear regression with global cognition (13-item Alzheimer's Disease Assessment Scale-cognitive subscale) as an independent variable of interest, and either gray matter volumes or white matter hyperintensity volume as dependent variables. These W scores, reflecting whether an individual's degree of cerebral damage is lower or higher than clinically expected, were tested as predictors of diagnostic conversion (i.e., NC to MCI/AD dementia, or MCI to AD dementia) and longitudinal changes in memory (ADNI-MEM) and executive functions (ADNI-EF). The median follow-up period was 24 months (interquartile range 6-42). Corrected for age, sex, Among Aβ-positive individuals, greater CR related to attenuated clinical progression in predementia stages of AD, but accelerated cognitive decline after the onset of dementia.
Identifiants
pubmed: 31266904
pii: WNL.0000000000007821
doi: 10.1212/WNL.0000000000007821
pmc: PMC6669930
doi:
Substances chimiques
2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole
0
Amyloid beta-Peptides
0
Aniline Compounds
0
Contrast Media
0
Ethylene Glycols
0
Peptide Fragments
0
Thiazoles
0
amyloid beta-protein (1-42)
0
florbetapir
6867Q6IKOD
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e334-e346Subventions
Organisme : NIA NIH HHS
ID : U01 AG024904
Pays : United States
Informations de copyright
Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.
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