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.
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