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Physical activity reduces amyloid‐induced neurodegeneration in non‐demented older adults
Author(s) -
Sohn Bo Kyung,
Yi Dahyun,
Byun Min Soo,
Jeon So Yeon,
Lee Jun Ho,
Lee Dong Woo,
Lee JunYoung,
Kim Yu Kyeong,
Sohn ChulHo,
Lee Dong Young
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.045939
Subject(s) - neurodegeneration , cognitive decline , pittsburgh compound b , positron emission tomography , neuroimaging , alzheimer's disease , medicine , psychology , dementia , cognition , neuroscience , disease
Background Both physical activity (PA) and cognitive activity (CA) are known to reduce the risk of Alzheimer`s disease (AD) and related cognitive decline. However, pathophysiological mechanism underlying their protective effects for AD is still poorly understood. We aimed to investigate the moderation effects of current PA and CA on the relationship between amyloid‐beta (Aβ) and AD‐signature neurodegeneration in non‐demented older adults. Both physical activity (PA) and cognitive activity (CA) are known to reduce the risk of Alzheimer`s disease (AD) and related cognitive decline. However, pathophysiological mechanism underlying their protective effects for AD is still poorly understood. We aimed to investigate the moderation effects of current PA and CA on the relationship between amyloid‐beta (Aβ) and AD‐signature neurodegeneration in non‐demented older adults. Method Two‐hundred sixty non‐demented (195 cognitively normal and 65 mild cognitive impairment) participants from the Korean Brain Aging Study for Early diagnosis and prediction of Alzheimer’s disease (KBASE) were included in this analysis. All participants underwent comprehensive clinical and neuropsychological assessment, [ 11 C]Pittsburgh Compound B (PiB) positron emission tomography (PET), [ 18 F]fluorodeoxyglucose (FDG) PET, and magnetic resonance imaging. Using the multi‐modal brain imaging data, in vivo AD pathologies including Aβ deposition, AD‐signature region cerebral glucose metabolism (AD‐CM), and AD‐signature region cortical thickness (AD‐CT) were quantified. Current PA and CA were assessed using well‐validated questionnaires. General linear model analysis was conducted including AD‐CM (or AD‐CT) as a dependent variable and Aβ deposition, PA, CA, Aβ x PA interaction term, and Aβ x CA interaction term as independent variables. Result We found significant Aβ x PA interaction effect on both AD‐CM and AD‐CT. Subgroup analyses showed that the inverse association between Aβ and AD‐CM (or AD‐CT) was weaker (i.e., smaller effect size) in higher PA group compared to that in lower PA group. In contrast, Aβ x CA interaction effect was not observed on neither AD‐CM nor AD‐CT. Conclusion The findings suggest that current PA reduce AD‐type regional neurodegeneration induced by Aβ deposition, regardless of CA, in non‐demented older adults. When considered with PA, however, current CA appear not have any moderation effect on the relationship of Aβ deposition with the neurodegenerative change.