STARRING ROLE OF MITOCHONDRIAL IMPAIRMENT IN ALZHEIMER’S DISEASE NEUROPATHOLOGY

Abstract

Alzheimer’s disease is the leading predominant demyelinating and degenerative ailment, described by the loss of cognitive function because of advanced neuronal loss in the brain. There are two pathological hallmarks in the brains of AD sufferers. One is the buildup of abnormal Tau proteins in neurons and the other is the formation of amyloid plaques. Although we still don’t know the comprehensive mechanism that is involved in AD pathophysiology; there are enormous studies that suggested thatmalfunctioning of mitochondria plays a substantial function in the pathology of AD. As we know that mitochondria are very dynamic organelles and the powerhouse of the cell (generate ATP). And it is said that a healthy pool of mitochondria is very essential because it provides energy to the neurons to perform the most important functions and it also protects the neurons by reducing the oxidative damage related to mitochondria. These organelles also play many important cellular functions such asregulation of intracellular calcium ions, bioenergetics processes, a scavenging system for free radicals, and stimulation of cell death that is mediated by caspases. But these functions can be adversely affected by amyloid beta-mediated mitochondrial dysfunction. In this article, I recapitulated the current advancement that highlights the starring role of mitochondrial impairment in AD pathology and summarize how different types of mechanisms are involved in mitochondrial impairment in thepathophysiology of AD.