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.
Keywords: Alzheimer disease, antioxidants, cerebrovascular pathology, mitochondria, neurodegeneration, oxidative stress.
Current Medicinal Chemistry
Title:Oxidative Stress Mediated Mitochondrial and Vascular Lesions as Markers in the Pathogenesis of Alzheimer Disease
Volume: 21 Issue: 19
Author(s): G. Aliev, M. Priyadarshini, V. P. Reddy, N.H. Grieg, Y. Kaminsky, R. Cacabelos, G. Md Ashraf, N.R. Jabir, M.A. Kamal, V.N. Nikolenko, A.A. Zamyatnin Jr., V. V. Benberin and S.O. Bachurin
Affiliation:
Keywords: Alzheimer disease, antioxidants, cerebrovascular pathology, mitochondria, neurodegeneration, oxidative stress.
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.
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Cite this article as:
Aliev G., Priyadarshini M., Reddy P. V., Grieg N.H., Kaminsky Y., Cacabelos R., Ashraf Md G., Jabir N.R., Kamal M.A., Nikolenko V.N., Jr. Zamyatnin A.A., Benberin V. V. and Bachurin S.O., Oxidative Stress Mediated Mitochondrial and Vascular Lesions as Markers in the Pathogenesis of Alzheimer Disease, Current Medicinal Chemistry 2014; 21 (19) . https://dx.doi.org/10.2174/0929867321666131227161303
DOI https://dx.doi.org/10.2174/0929867321666131227161303 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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