A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Cortical beta-amyloid burden, gray matter, and memory in adults at varying APOE epsilon 4 risk for Alzheimer's disease
Tekijät: Mecca AP, Barcelos NM, Wang S, Bruck A, Nabulsi N, Planeta-Wilson B, Nadelmann J, Benincasa AL, Ropchan J, Huang YY, Gelernter J, Van Ness PH, Carson RE, van Dyck CH
Kustantaja: ELSEVIER SCIENCE INC
Julkaisuvuosi: 2018
Journal: Neurobiology of Aging
Tietokannassa oleva lehden nimi: NEUROBIOLOGY OF AGING
Lehden akronyymi: NEUROBIOL AGING
Vuosikerta: 61
Aloitussivu: 207
Lopetussivu: 214
Sivujen määrä: 8
ISSN: 0197-4580
DOI: https://doi.org/10.1016/j.neurobiolaging.2017.09.027
Tiivistelmä
Models of preclinical Alzheimer's disease (AD) propose that cerebral amyloidosis leads to neuro-degeneration and subsequent cognitive decline. This study investigated whether APOE genotype is related to beta-amyloid (A beta) burden in brain regions preferentially affected by AD and whether A beta burden is associated with gray-matter (GM) fraction (as a marker of neurodegeneration) and episodic memory performance in cognitively normal middle-aged individuals at varying genetic risk for AD. Three groups of cognitively normal participants aged 50-65 years with a first-degree family history of AD (APOE genotype epsilon 4 epsilon 4 [n = 15], epsilon 3 epsilon 4 [n = 15], and epsilon 3 epsilon 3 [n = 15]) underwent [C-11]PiB positron emission tomography scans to quantify cortical A beta, brain magnetic resonance imaging, and neuropsychological testing. APOE epsilon 4 epsilon 4 participants demonstrated significantly higher cortical A beta burden than APOE epsilon 3 epsilon 3 (p < 0.001). Furthermore, cortical A beta burden was inversely associated with cortical GM fraction (p = 0.017) but not episodic memory performance. In cognitively normal, middle-aged individuals, A beta burden is significantly associated with GM fraction but not episodic memory performance. These findings are consistent with models of preclinical AD in which neurodegeneration occurs before manifest cognitive decline. (C) 2017 The Authors. Published by Elsevier Inc.
Models of preclinical Alzheimer's disease (AD) propose that cerebral amyloidosis leads to neuro-degeneration and subsequent cognitive decline. This study investigated whether APOE genotype is related to beta-amyloid (A beta) burden in brain regions preferentially affected by AD and whether A beta burden is associated with gray-matter (GM) fraction (as a marker of neurodegeneration) and episodic memory performance in cognitively normal middle-aged individuals at varying genetic risk for AD. Three groups of cognitively normal participants aged 50-65 years with a first-degree family history of AD (APOE genotype epsilon 4 epsilon 4 [n = 15], epsilon 3 epsilon 4 [n = 15], and epsilon 3 epsilon 3 [n = 15]) underwent [C-11]PiB positron emission tomography scans to quantify cortical A beta, brain magnetic resonance imaging, and neuropsychological testing. APOE epsilon 4 epsilon 4 participants demonstrated significantly higher cortical A beta burden than APOE epsilon 3 epsilon 3 (p < 0.001). Furthermore, cortical A beta burden was inversely associated with cortical GM fraction (p = 0.017) but not episodic memory performance. In cognitively normal, middle-aged individuals, A beta burden is significantly associated with GM fraction but not episodic memory performance. These findings are consistent with models of preclinical AD in which neurodegeneration occurs before manifest cognitive decline. (C) 2017 The Authors. Published by Elsevier Inc.
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