Document Detail


Stress, exercise, and Alzheimer's disease: a neurovascular pathway.
MedLine Citation:
PMID:  21398043     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Genetic factors are known to play a role in Alzheimer's disease (AD) vulnerability, yet less than 1% of incident AD cases are directly linked to genetic causes, suggesting that environmental variables likely play a role in the majority of cases. Several recent human and animal studies have examined the effects of behavioral factors, specifically psychological stress and exercise, on AD vulnerability. Numerous animal studies have found that, while stress exacerbates neuropathological changes associated with AD, exercise reduces these changes. Some human studies suggest that psychological stress can increase the risk of developing AD, while other studies suggest that exercise can significantly reduce AD risk. Most animal studies investigating the mechanisms responsible for the effects of these behavioral factors have focused on neuronal processes, including the effects of stress hormones and neurotrophic factors on the neuropathological hallmarks of AD, namely amyloid-beta (Aβ) deposition and tau-phosphorylation. However, cumulative evidence indicates that, in humans, AD is associated with the presence of cerebrovascular disease, and cardiovascular risk factors are associated with increased risk of developing AD. There is an extensive literature demonstrating that behavioral factors, particularly stress and exercise, can powerfully modulate the pathophysiology of vascular disease. Thus, the following model proposes that the influence of stress and exercise on AD risk may be partially due to the effects of these behavioral factors on vascular homeostasis and pathology. These effects are likely due to both indirect modification of AD risk through alterations in vascular risk factors, such as hypertension, diabetes, and aortic stiffening, as well as direct influence on the cerebrovasculature, including changes in cerebral blood flow, angiogenesis, and vascular disease. Future studies examining the effects of behavioral factors on AD risk should incorporate measures of both peripheral and cerebral vascular function to further our understanding of the mechanisms by which behavior can modify AD susceptibility. Greater knowledge of the molecular mechanisms behind these behavioral effects would further our understanding of the disease and lead to innovative treatment and preventive approaches.
Authors:
Daniel A Nation; Suzi Hong; Amy J Jak; Lisa Delano-Wood; Paul J Mills; Mark W Bondi; Joel E Dimsdale
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2011-03-12
Journal Detail:
Title:  Medical hypotheses     Volume:  76     ISSN:  1532-2777     ISO Abbreviation:  Med. Hypotheses     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-13     Completed Date:  2011-09-15     Revised Date:  2014-09-09    
Medline Journal Info:
Nlm Unique ID:  7505668     Medline TA:  Med Hypotheses     Country:  United States    
Other Details:
Languages:  eng     Pagination:  847-54     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ltd. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Alzheimer Disease / physiopathology*
Exercise*
Humans
Models, Theoretical
Oxidative Stress
Risk Factors
Stress, Psychological*
Grant Support
ID/Acronym/Agency:
K24 AG026431/AG/NIA NIH HHS; K24 AG026431/AG/NIA NIH HHS; K24 AG026431-05/AG/NIA NIH HHS; MH18399/MH/NIMH NIH HHS; R01 AG012674/AG/NIA NIH HHS; R01 AG012674/AG/NIA NIH HHS; R01 AG012674-14/AG/NIA NIH HHS; R01 HL-073355/HL/NHLBI NIH HHS; R01 HL091848-01A1/HL/NHLBI NIH HHS; R01 HL36005-20A1/HL/NHLBI NIH HHS; R01 HL44915-13A1/HL/NHLBI NIH HHS; R01 HL57265/HL/NHLBI NIH HHS; R01 HL90975/HL/NHLBI NIH HHS
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