A molecular mechanism contributing to mitochondrial dysfunction and Alzheimer’s disease
Alzheimer's disease (AD) is a devastating neurological disorder that results in significant cognitive impairment and memory loss. A common feature in late onset AD patients is the accumulation of amyloid plaques in the brain. These plaques are clusters of amyloid precursor protein fragments that form in neurons. Despite years of research, the molecular mechanisms that contribute to the formation of amyloid plaques remain unknown and multiple hypotheses for their origin have been proposed. A common thread in AD research is the hypothesis that mitochondrial dysfunction plays a role in the formation of amyloid plaques. This invention identifies a molecular mechanism that can contribute to mitochondrial dysfunction in age-related neurological disorders and helps to explain the formation of amyloid plaques in AD patients. A therapeutic approach to prevent mitochondrial dysfunction is presented.