MITOCHONDRIAL DYSFUNCTION IN THE PATHOGENESIS OF ALZHEIMER’S DISEASE: A REVIEW
Maitrayee Banerjee Mukherjee*
Alzheimer’s Disease (AD) is a type of dementia that causes loss of memory, cognitive impairment and development of some non cognitive features such as myoclonus, seizures etc. Biomarkers of important categories of neuropathologic change of AD, i.e., β-amyloid (Aβ) deposition, pathologic tau, and neurodegeneration, have been developed. Although AD is defined on the basis of amyloid-β plaque and tau neurofibrillary tangle deposition within the neocortex but the biochemical and metabolic changes in the brain that characterize the disease remain incompletely understood. The functional and metabolic changes of mitochondria in both the nervous tissue and rest of the body is observed early in this disease, and both amyloid and tau have detrimental effects on mitochondrial function. ROS generated cause damages in mitochondrial DNA (mtDNA) and other mitochondrial components, inducing a dysfunctional mitochondrial state. These include mitochondrial DNA damage, dysfunctional mitochondrial DNA expression, increased mitochondrial DNA mutations, reduced mitochondrial DNA copies, increased oxidative damage, reduced mitochondrial axonal transport, and overall impaired mitochondrial dynamics In this review article, various changes in the function and structure of mitochondria and its role in the pathogenesis of AD is discussed.
Keywords: Dementia, Alzheimer’s Disease, Mitochondria DNA , Mutation.
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