Molecular basis of the development of Parkinson's disease.

Abstract

Parkinson's disease is one of the most prevalent neurodegenerative motor disorders worldwide with postural instability, bradykinesia, resting tremor and rigidity being the most common symptoms of the disease. Despite the fact that the molecular mechanisms of Parkinson's disease pathogenesis have already been well described, there is still no coherent picture of the etiopathogenesis of this disease. According to modern concepts, neurodegeneration is induced mainly by oxidative stress, neuroinflammation, dysregulation of cerebral proteostasis, apoptotic dysregulation, and impaired autophagy. This review describes how various factors contribute to neurodegeneration in Parkinson's disease. Understanding the factors affecting fundamental cellular processes and responsible for disease progression may help develop therapeutic strategies to improve the quality of life of patients suffering from the disease. The review also discusses the role of calpains in the development of Parkinson's disease. It is known that α-synuclein is a substrate of calcium-dependent proteases of the calpain family. Truncated forms of α-synuclein are not only involved in the process of formation of the aggregates, but also increase their toxicity.