CoQ10 and Mitochondrial Dysfunction in Alzheimer's Disease
Status PubMed-not-MEDLINE Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články, přehledy
Grantová podpora
Cooperatio
Charles University
MH CZ-DRO VFN64165
General University Hospital in Prague
NU23-04-00032
Ministry of Health Czech Republic
PubMed
38397789
PubMed Central
PMC10885987
DOI
10.3390/antiox13020191
PII: antiox13020191
Knihovny.cz E-zdroje
- Klíčová slova
- Alzheimer’s disease, coenzyme Q10, drug, mitochondrial dysfunction, oxidative stress,
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
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.
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