We need to move more: Neurobiological hypotheses of physical exercise as a treatment for Parkinson's disease

Abstract

Parkinson's disease (PD) is one of the most prevalent neurodegenerative diseases in the world. The degeneration of dopaminergic neurons in the substantia nigra and chronic inflammation impair specific brain areas, which in turn result in lesser motor control, behavioral changes and cognitive decline. Nowadays, drug-treatments are the foremost approaches in treating PD. However, exercise has been shown to have powerful effects on PD, based on several neurobiological mechanisms. These effects may decrease the risk of developing PD by 33%. However, these mechanisms are unclear and little explored. Among several mechanisms, we propose two specific hypotheses: 1. Physical exercise reduces chronic oxidative stress and stimulates mitochondria biogenesis and up-regulation of authophagy in PD patients. Moreover, antioxidant enzymes (e.g. superoxide dismutase) become more active and effective in response to physical exercise. 2. Exercise stimulates neurotransmitter (e.g. dopamine) and trophic factors (BDNF, GDNF, FGF-2, IGF-1, among others) synthesis. These neurochemical phenomena promote neuroplasticity, which, in turn, decreases neural apoptosis and may delay the neurodegeneration process, preventing or decreasing PD development and symptoms, respectively.