Abstract
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.
Keywords: Alzheimer disease, Ischemia, Mitochondria, mtDNA, Neurodegeneration, Oxidative stress, ROS
Current Neurovascular Research
Title:Vascular Factors and Mitochondrial Dysfunction: a Central Role in the Pathogenesis of Alzheimer’s Disease
Volume: 10 Issue: 1
Author(s): Daniele Orsucci, Michelangelo Mancuso, Elena Caldarazzo Ienco, Costanza Simoncini, Gabriele Siciliano and Ubaldo Bonuccelli
Affiliation:
Keywords: Alzheimer disease, Ischemia, Mitochondria, mtDNA, Neurodegeneration, Oxidative stress, ROS
Abstract: 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.
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Cite this article as:
Orsucci Daniele, Mancuso Michelangelo, Caldarazzo Ienco Elena, Simoncini Costanza, Siciliano Gabriele and Bonuccelli Ubaldo, Vascular Factors and Mitochondrial Dysfunction: a Central Role in the Pathogenesis of Alzheimer’s Disease, Current Neurovascular Research 2013; 10 (1) . https://dx.doi.org/10.2174/1567202611310010010
DOI https://dx.doi.org/10.2174/1567202611310010010 |
Print ISSN 1567-2026 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5739 |
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