Impaired Mitophagy and Mitochondrial Function in Alzheimer ' s Disease

Alzheimer's disease starts with an accumulation of amyloid-β, which disrupts cellular metabolism sufficiently to lay the grounds for the chronic inflammation and aggregation of tau protein that characterize the later, severe stage of the condition. Here, researchers make the argument that a fair degree of this progression is mediated via dysfunction of mitochondria and the quality control mechanisms of mitophagy, normally responsible for removing damaged mitochondria, and that this dysfunction is caused by amyloid-β. Mitochondria are the power plants of the cell, and a faltering of their activity has profoundly disruptive effects. Needless to say, mitochondrial dysfunction is a characteristic feature of aging. This leads to the point that aging is a complex enough phenomenon for it to be possible to argue that mitochondrial dysfunction contributes to amyloid-β and tau aggregation, not vice versa. Or that both directions of causation are real phenomena. These are not simple, easily modeled systems. The fastest way to a definitive answer is likely that of building rejuvenation therapies capable of restoring mitochondrial function to youthful levels, and observing the result. Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by memory loss and multiple cognitive impairments. Several decades of intense research have revealed that multiple cellular changes are implicated in the development and progression of AD, including mitochon...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs