CoQ10 and Mitochondrial Dysfunction in Alzheimer’s Disease

Abstract

The progress in understanding the pathogenesis and treatment of Alzheimer’s disease (AD) is based on the recognition of the primary causes of the disease, which can be deduced from the knowledge of risk factors and biomarkers measurable in the early stages of the disease. Insights into the risk factors and the time course of biomarker abnormalities point to a role for the connection of amyloid beta (Aβ) pathology, tau pathology, mitochondrial dysfunction, and oxidative stress in the onset and development of AD. Coenzyme Q10 (CoQ10) is a lipid antioxidant and electron transporter in the mitochondrial electron transport system. The availability and activity of CoQ10 is crucial for proper mitochondrial function and cellular bioenergetics. Based on the mitochondrial hypothesis of AD and the hypothesis of oxidative stress, the regulation of the efficiency of the oxidative phosphorylation system by means of CoQ10 can be considered promising in restoring the mitochondrial function impaired in AD, or in preventing the onset of mitochondrial dysfunction and the development of amyloid and tau pathology in AD. This review summarizes the knowledge on the pathophysiology of AD, in which CoQ10 may play a significant role, with the aim of evaluating the perspective of the pharmacotherapy of AD with CoQ10 and its analogues.

Infectious viruses and neurodegenerative diseases: The mitochondrial defect hypothesis

“…However, hydrogen peroxide can cross the membrane and transform into the highly reactive hydroxyl radical in the cytoplasm, causing irreversible protein, lipid, and DNA damage. 24 Consequently, mitochondrial stress significantly accelerates microglial cell senescence.…”