Cerebral amyloidosis associated with cognitive decline in autosomal dominant Alzheimer disease

Autor: Wang, Fen, Gordon, Brian A, McDade, Eric, Ringman, John M, Graff-Radford, Neill R, Ghetti, Bernardino, Farlow, Martin R, Sperling, Reisa, Salloway, Steve, Schofield, Peter R, Masters, Colin L, Martins, Ralph N, Ryman, Davis C, Rossor, Martin N, Jucker, Mathias, Danek, Adrian, Förster, Stefan, Lane, Christopher A S, Morris, John C, Benzinger, Tammie L S, Bateman, Randall J, Network, Dominantly Inherited Alzheimer, Ma, Shengmei, Xiong, Chengjie, Hassenstab, Jason, Goate, Alison, Fagan, Anne M, Cairns, Nigel J, Marcus, Daniel S
Rok vydání: 2014
Předmět:
Male
Pediatrics
psychology [Alzheimer Disease]
psychology [Amyloidosis]
Apolipoprotein E4
genetics [Alzheimer Disease]
Neuropsychological Tests
diagnostic imaging [Cognition Disorders]
APP protein
human

Developmental psychology
Amyloid beta-Protein Precursor
psychology [Brain Diseases]
Longitudinal Studies
Cognitive decline
Episodic memory
genetics [Apolipoprotein E4]
Brain Diseases
Amyloidosis
physiopathology [Amyloidosis]
Neuropsychology
Brain
Cognition
genetics [Presenilin-1]
Middle Aged
genetics [Amyloid beta-Protein Precursor]
Disease Progression
Female
diagnostic imaging [Brain Diseases]
Alzheimer's disease
Psychology
Adult
medicine.medical_specialty
diagnostic imaging [Amyloidosis]
genetics [Presenilin-2]
physiopathology [Alzheimer Disease]
PSEN1 protein
human

Alzheimer Disease
Presenilin-2
medicine
Presenilin-1
Dementia
Humans
ddc:610
Effects of sleep deprivation on cognitive performance
Radionuclide Imaging
diagnostic imaging [Brain]
PSEN2 protein
human

medicine.disease
Cross-Sectional Studies
physiopathology [Brain Diseases]
Neurology (clinical)
Cognition Disorders
diagnostic imaging [Alzheimer Disease]
Follow-Up Studies
Zdroj: Neurology 85(9), 790-798 (2015). doi:10.1212/WNL.0000000000001903
ISSN: 1526-632X
DOI: 10.1212/WNL.0000000000001903
Popis: Objective: To investigate the associations of cerebral amyloidosis with concurrent cognitive performance and with longitudinal cognitive decline in asymptomatic and symptomatic stages of autosomal dominant Alzheimer disease (ADAD). Methods: Two hundred sixty-three participants enrolled in the Dominantly Inherited Alzheimer Network observational study underwent neuropsychological evaluation as well as PET scans with Pittsburgh compound B. One hundred twenty-one participants completed at least 1 follow-up neuropsychological evaluation. Four composite cognitive measures representing global cognition, episodic memory, language, and working memory were generated using z scores from a battery of 13 standard neuropsychological tests. General linear mixed-effects models were used to investigate the relationship between baseline cerebral amyloidosis and baseline cognitive performance and whether baseline cerebral amyloidosis predicts cognitive change over time (mean follow-up 2.32 years ± 0.92, range 0.89–4.19) after controlling for estimated years from expected symptom onset, APOE e4 allelic status, and education. Results: In asymptomatic mutation carriers, amyloid burden was not associated with baseline cognitive functioning but was significantly predictive of longitudinal decline in episodic memory. In symptomatic mutation carriers, cerebral amyloidosis was correlated with worse baseline performance in multiple cognitive composites and predicted greater decline over time in global cognition, working memory, and Mini-Mental State Examination. Conclusions: Cerebral amyloidosis predicts longitudinal episodic memory decline in presymptomatic ADAD and multidomain cognitive decline in symptomatic ADAD. These findings imply that amyloidosis in the brain is an indicator of early cognitive decline and provides a useful outcome measure for early assessment and prevention treatment trials.
Databáze: OpenAIRE