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Physical Activity and Amyloid‐ β Brain Levels in Elderly Adults with Intact Cognition and Mild Cognitive Impairment
Author(s) -
Souto Barreto Philipe,
Andrieu Sandrine,
Payoux Pierre,
Demougeot Laurent,
Rolland Yves,
Vellas Bruno
Publication year - 2015
Publication title -
journal of the american geriatrics society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.992
H-Index - 232
eISSN - 1532-5415
pISSN - 0002-8614
DOI - 10.1111/jgs.13530
Subject(s) - medicine , dementia , pittsburgh compound b , standardized uptake value , cognition , positron emission tomography , cognitive impairment , amyloid (mycology) , gerontology , cardiology , disease , pathology , nuclear medicine , psychiatry
Objectives To examine the associations between amyloid‐ β brain deposition and physical activity ( PA ) in elderly adults without dementia and to investigate whether the association has a dose‐response relationship. Design Cross‐sectional study. Setting French community‐dwelling people. Participants Elderly adults with normal or mildly impaired cognition (mean age 74.7 ± 4.2; 60.4% female) with available information on current self‐reported PA and amyloid‐ β brain deposition measured using positron emission tomography ( PET ) using the PET ‐ligand florbetapir F 18 (n = 268). Measurements A standardized uptake value ratio ( SUVR ) was obtained for each subject. Participants were divided according to amyloid plaque cortical retention defined according to a SUVR cutoff of 1.10 ( SUVR + vs SUVR −). Results Bivariate and multivariate analyses showed that PA was not significantly associated with SUVR . SUVR + and SUVR − participants did not differ in terms of volume (continuous PA variables) and levels (categorical PA variables) of PA . PA was not correlated with SUVR in apolipoprotein E ε 4 carriers or noncarriers. PA was not associated with cognitive function. Conclusion Although PA protects against dementia, there is no solid evidence that this protection involves a reduction in amyloid‐ β brain deposition. Further studies are needed to determine whether PA (ideally measured at several time‐points using objective measures) is involved in the pathophysiology of Alzheimer's disease.

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