Brown, BM;
Sohrabi, HR;
Taddei, K;
Gardener, SL;
Rainey-Smith, SR;
Peiffer, JJ;
Xiong, C;
... Martins, RN; + view all
(2017)
Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease.
Alzheimer's & Dementia
, 13
(11)
pp. 1197-1206.
10.1016/j.jalz.2017.03.008.
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Abstract
INTRODUCTION: The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. METHODS: In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42, and CSF tau levels was evaluated using linear regression. RESULTS: No differences in brain amyloid load, CSF Aβ42, or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. DISCUSSION: Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers.
Type: | Article |
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Title: | Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease |
Open access status: | An open access version is available from UCL Discovery |
DOI: | 10.1016/j.jalz.2017.03.008 |
Publisher version: | http://dx.doi.org/10.1016/j.jalz.2017.03.008 |
Language: | English |
Additional information: | This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions. |
Keywords: | Science & Technology, Life Sciences & Biomedicine, Clinical Neurology, Neurosciences & Neurology, Physical activity, Amyloid beta, Genetics, Tau, Alzheimer's disease, Dementia, APP/PS1 TRANSGENIC MICE, PHYSICAL-ACTIVITY, A-BETA, COGNITIVE DECLINE, OLDER-ADULTS, MOUSE MODEL, BIOMARKERS, DEPOSITION, RISK, VOLUNTARY |
UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Neurodegenerative Diseases |
URI: | https://discovery.ucl.ac.uk/id/eprint/10044174 |
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