Mitochondrial dysfunction and oxidative stress in Alzheimer's disease–A step towards mitochondria based therapeutic strategies

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease with reduced cognitive function due to mitochondrial dysfunction and oxidative stress. Recent studies show that the pathophysiology of AD may be influenced by mitochondrial dysfunctionality, Ca2+ imbalance, apoptosis, decreased energy, and alteration in its metabolism. Study indicates that damaged mitochondria play critical roles in the pathogenesis of AD, even if the precise mechanism behind AD pathogenesis remains unknown. It is thought that a healthy pool of mitochondria protects neurons by reducing oxidative damage caused by mitochondria and also promotes neuronal activity by giving neurons enough energy and other associated mitochondrial functions. In this sense, investigation of the mitochondrial mechanisms that altered the pathogenesis of AD constitutes novel, promising therapeutic targets for the disease. Mitochondria enhances energy generation, antioxidants to scavenge reactive oxygen species and reduce oxidative damage substrate supply, glucose metabolism, and potential drug candidates that target apoptotic and mitophagy pathways to remove damaged mitochondria. Although mitochondrial therapy approaches have shown promise in preclinical studies, there hasn't been much advancement in clinical trials thus far. Therefore, we try to find out the role of mitochondria in AD and highlight the development of compounds that target mitochondria as potential therapeutic targets for AD.