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.

• Klíčová slova
• Alzheimer’s disease, coenzyme Q10, drug, mitochondrial dysfunction, oxidative stress,
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

The disease progression of neurodegenerative disorders (NDD), including Alzheimer's, Parkinson's and Huntington's disease, is inextricably tied to mitochondrial dysfunction. However, although the contribution by nuclear gene mutations is recognised for familial onset of NDD, the degree to which cytoplasmic inheritance serves as a predetermining factor for the predisposition and onset of NDD is not yet fully understood. We review the reproductive mechanisms responsible for ensuring a healthy mitochondrial population within each new generation and elucidate how advanced maternal age can constitute an increased risk for the onset of NDD in the offspring, through the increased heteroplasmic burden. On the one hand, this review draws attention to how assisted reproductive technologies (ART) can impair mitochondrial fitness in offspring. On the other hand, we consider qualified ART approaches as a significant tool for the prevention of NDD pathogenesis.

• MeSH
• cvičení MeSH
• lidé MeSH
• mitochondrie genetika   MeSH
• neurodegenerativní nemoci * genetika   MeSH
• progrese nemoci MeSH
• rozmnožování MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH