Dysfunction of mitochondria: Implications for Alzheimer's disease

Abstract

Alzheimer's disease (AD), the most common form of dementia, is thought to be associated with multiple factors, where the greatest risk factor is aging. Several traditional views attribute the cause of AD to genetic heritability, reduced synthesis of the neurotransmitter acetylcholine, the accumulation of a toxic protein known as amyloid β (Aβ) peptide, and/or neurofibrillary tangles of hyperphosphorylated tau-protein, which affect microtubule stability. However, with several recent clinical trial failures involving billions of dollars of revenue, traditional views are being questioned more each day. New theories involving metabolic activity and mitochondrial dysfunction, which proposes that altered mitochondria are the driving force for the development of AD, are being examined and investigated more critically. Understanding mitochondrial dysfunction and therapeutically targeting mitochondrial bioenergetics in AD could be a novel treatment approach holding great promise for preventing and/or slowing the onset of AD.

Keywords: ATP; Alzheimer's disease; Bioenergetics; Dementia; Memory; Mitochondrion; Neurodegeneration; Neurology.