Document Detail

Vascular factors and mitochondrial dysfunction: a central role in the pathogenesis of Alzheimer's disease.
MedLine Citation:
PMID:  23151073     Owner:  NLM     Status:  MEDLINE    
The pathogenesis of Alzheimer's disease (AD) is complex, and only a minority of cases appears to be primarily genetic. A relationship between genetic and acquired vascular factors in AD has been hypothesized. Many vascular risk factors for AD, such as atherosclerosis, stroke and cardiac disease in the aging individual, could result in cerebrovascular dysfunction. A major vascular susceptibility factor gene is the apolipoprotein E gene, found to be associated with sporadic late-onset AD cases. Oxidative damage and mitochondrial dysfunction have been also implicated in the pathogenesis of AD, but the question as to whether they are involved in the onset and progression of the pathology or rather represent a consequence of neurodegeneration is still debated. Recent evidence suggests that chronic hypoperfusion may trigger mitochondrial dysfunction in vascular cells which, in turn, may enhance the production of reactive oxygen species. In this short review we revise the link between vascular factors and mitochondrial dysfunction in AD pathogenesis.
Daniele Orsucci; Michelangelo Mancuso; Elena Caldarazzo Ienco; Costanza Simoncini; Gabriele Siciliano; Ubaldo Bonuccelli
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current neurovascular research     Volume:  10     ISSN:  1875-5739     ISO Abbreviation:  Curr Neurovasc Res     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-02-08     Completed Date:  2013-07-29     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  101208439     Medline TA:  Curr Neurovasc Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  76-80     Citation Subset:  IM    
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MeSH Terms
Aging / metabolism,  pathology
Alzheimer Disease / etiology*,  metabolism,  pathology,  physiopathology
Brain / metabolism*,  pathology,  physiopathology
Mitochondria / metabolism*,  pathology
Oxidative Stress / physiology*
Reactive Oxygen Species / metabolism*
Grant Support
Reg. No./Substance:
0/Reactive Oxygen Species

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