Effect of lifestyle activities on Alzheimer disease biomarkers and cognition

生活方式活动对阿尔茨海默病生物标志物和认知能力的影响

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Abstract

OBJECTIVE: A study was undertaken to investigate the association of intellectual and physical activity with biomarkers of Alzheimer disease (AD) pathophysiology and cognition in a nondemented elderly population. The biomarkers evaluated were brain Aβ load via Pittsburgh compound B (PiB)-positron emission tomography (PET), neuronal dysfunction via (18) F-fluorodeoxyglucose (FDG)-PET, and neurodegeneration via structural magnetic resonance imaging (MRI). METHODS: We studied 515 nondemented (428 cognitively normal and 87 mild cognitive impairment) participants in the population-based Mayo Clinic Study of Aging who completed a 3T MRI, PET scans, and APOE genotype, and had lifestyle activity measures and cognition data available. The imaging measures computed were global PiB-PET uptake, and global FDG-PET and MRI based hippocampal volume. We consolidated activity variables into lifetime intellectual, current intellectual, and current physical activities. We used a global cognitive z score as a measure of cognition. We applied 2 independent methods-partial correlation analysis adjusted for age and gender and path analysis using structural equations-to evaluate the associations between lifestyle activities, imaging biomarkers, and global cognition. RESULTS: None of the lifestyle variables were correlated with the biomarkers, and the path associations between lifestyle variables and biomarkers were not significant (p > 0.05). Conversely, all the biomarkers were correlated with global cognitive z score (p < 0.05), and the path associations between (lifetime and current) intellectual activities and global z score were significant (p < 0.01). INTERPRETATION: Intellectual and physical activity lifestyle factors were not associated with AD biomarkers, but intellectual lifestyle factors explained variability in the cognitive performance in this nondemented population. This study provides evidence that lifestyle activities may delay the onset of dementia but do not significantly influence the expression of AD pathophysiology.

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