Mitochondrial Dysfunction in the Pathogenesis of Parkinson Disease: Current Concepts and Potential Therapeutic Strategies
Mitochondrial Dysfunction in the Pathogenesis of Parkinson Disease: Current Concepts and Potential Therapeutic Strategies
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
A plain-language reading has not been prepared for this paper yet.
Original abstract
Parkinson disease (PD) is a progressive extrapyramidal disorder characterized by the biodegradation of dopaminergic neurons in the substantia nigra. The total number of patients diagnosed with PD worldwide is expected to more than double by 2030, inevitably placing a significant financial burden on healthcare systems. The progression of the disease leads to persistent maladjustment in all aspects of the patient’s life, resulting in a loss of human resources. Approximately 85–90% of PD cases are sporadic and multifactorial. The remaining 10–15% are familial forms with conventional inheritance patterns. Current research suggests multiple mechanisms for PD development, but increasing evidence supports a critical role of mitochondrial dysfunction in PD pathogenesis. The aim of this review was to discuss the key pathogenetic mechanisms of mitochondrial dysfunction in PD pathogenesis. The following keywords and phrases (both in Russian and English) were used to search databases such as eLIBRARY.RU, PubMed, and Web of Science for full-text articles in Russian and English published over the last 20 years: Parkinson disease, neurodegeneration, pathophysiology, mitochondrial dysfunction, bioenergetics, mitophagy, pathogenetic therapy. The review describes the factors that cause mitochondrial dysfunction and its impact on PD. Potential therapeutic strategies targeting mitochondrial dysfunction are also described.