The Role of Exercise in Maintaining Mitochondrial Proteostasis in Parkinson’s Disease

Abstract

Parkinson’s disease (PD) is the second most common rapidly progressive neurodegenerative disease and has serious health and socio-economic consequences. Mitochondrial dysfunction is closely related to the onset and progression of PD, and the use of mitochondria as a target for PD therapy has been gaining traction in terms of both recognition and application. The disruption of mitochondrial proteostasis in the brain tissue of PD patients leads to mitochondrial dysfunction, which manifests as mitochondrial unfolded protein response, mitophagy, and mitochondrial oxidative phosphorylation. Physical exercise is important for the maintenance of human health, and has the great advantage of being a non-pharmacological therapy that is non-toxic, low-cost, and universally applicable. In this review, we investigate the relationships between exercise, mitochondrial proteostasis, and PD and explore the role and mechanisms of mitochondrial proteostasis in delaying PD through exercise.

Aging and Parkinson’s disease: a complex interplay of vulnerable neurons, the immune system and the blood-brain barrier

“…Especially striking in this context is the fact that stereotaxic, but also intravenous and intranasal transfer of allogenic mitochondria was associated with improvement in locomotor function and less degeneration of dopaminergic neurons in rodent models of PD [34][35][36] . Other non-pharmacological interventions like intermittent fasting and exercise that show promise in the treatment of PD have similarly been linked to enhanced mitochondrial biogenesis and the regulation of mitochondrial function [37][38][39][40] .…”

The Role of Cellular Defense Systems of Ferroptosis in Parkinson’s Disease and Alzheimer’s Disease

“…Parkinson’s disease (PD) and Alzheimer’s disease (AD) are the most common rapidly developing neurodegenerative diseases [ 1 , 2 , 3 , 4 ]. Ferroptosis is a non-apoptotic form of cell death: iron-dependent regulated necrosis occasioned by uncontrolled lipid peroxidation-mediated oxidative damage to the cell membrane [ 5 , 6 , 7 ].…”