Oxidative Stress Mediated Mitochondrial and Vascular Lesions as Markers in the Pathogenesis of Alzheimer Disease
Abstract
Mitochondrial dysfunction plausibly underlies the aging-associated brain degeneration. Mitochondria play a pivotal role in cellular bioenergetics and cell-survival. Oxidative stress consequent to chronic hypoperfusion induces mitochondrial damage, which is implicated as the primary cause of cerebrovascular accidents (CVA) mediated Alzheimer's disease (AD). The mitochondrial function deteriorates with aging, and the mitochondrial damage correlates with increased intracellular production of oxidants and pro-oxidants. The prolonged oxidative stress and the resultant hypoperfusion in the brain tissues stimulate the expression of nitric oxide synthase (NOS) enzymes, which further drives the formation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). The ROS and RNS collectively contributes to the dysfunction of the blood-brain barrier (BBB) and damage to the brain parenchymal cells. Delineating the molecular mechanisms of these processes may provide clues for the novel therapeutic targets for CVA and AD patients.
Recommended Citation
G. M. Aliev and M. Priyadarshini and P. Reddy and N. H. Grieg and Y. G. Kaminsky and R. Cacabelos and G. M. Ashraf and N. R. Jabir and M. A. Kamal and V. N. Nikolenko and A. A. Zamyatnin and V. V. Benberin and S. O. Bachurin, "Oxidative Stress Mediated Mitochondrial and Vascular Lesions as Markers in the Pathogenesis of Alzheimer Disease," Current Medicinal Chemistry, vol. 21, no. 19, pp. 2208 - 2217, Bentham Science Publishers B.V., Jan 2014.
The definitive version is available at https://doi.org/10.2174/0929867321666131227161303
Department(s)
Chemistry
Keywords and Phrases
Alzheimer disease; Antioxidants; Cerebrovascular pathology; Mitochondria; Neurodegeneration; Oxidative stress
International Standard Serial Number (ISSN)
0929-8673
Document Type
Article - Journal
Document Version
Citation
File Type
text
Language(s)
English
Rights
© 2014 Bentham Science Publishers B.V., All rights reserved.
Publication Date
01 Jan 2014
