| Autor: |
Aliev G, Priyadarshini M, Reddy VP, Grieg NH, Kaminsky Y, Cacabelos R, Ashraf GM, Jabir NR, Kamal MA, Nikolenko VN, Zamyatnin AA Jr, Benberin VV, Bachurin SO; ' GALLY' International Biomedical Research Consulting LLC, 7733 Louis Pasteur Drive, #330. San Antonio, TX, 78229, USA. aliev03@gmail.com. |
| Jazyk: |
angličtina |
| Zdroj: |
Current medicinal chemistry [Curr Med Chem] 2014; Vol. 21 (19), pp. 2208-17. |
| DOI: |
10.2174/0929867321666131227161303 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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