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CoQ10 and Mitochondrial Dysfunction in Alzheimer’s Disease
Version 1
: Received: 3 January 2024 / Approved: 4 January 2024 / Online: 4 January 2024 (03:33:56 CET)
A peer-reviewed article of this Preprint also exists.
Fišar, Z.; Hroudová, J. CoQ10 and Mitochondrial Dysfunction in Alzheimer’s Disease. Antioxidants 2024, 13, 191. Fišar, Z.; Hroudová, J. CoQ10 and Mitochondrial Dysfunction in Alzheimer’s Disease. Antioxidants 2024, 13, 191.
Abstract
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 risk factors and the time course of biomarker abnormalities point to a role for 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.
Keywords
Alzheimer’s disease; Coenzyme Q10; Mitochondrial dysfunction; Oxidative stress; Drug
Subject
Biology and Life Sciences, Neuroscience and Neurology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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