Swimming exercise reduces native ⍺-synuclein protein species in a transgenic C. elegans model of Parkinson’s disease.

Exercise has been historically recommended to prevent many disease conditions. Intense exercise in particular, has been shown to be beneficial for Parkinson’s disease (PD) — stopping and even reversing symptoms in some patients. Recent research in mammalian animal models of Parkinson’s have shown that exercise affects ⍺-synuclein aggregate species, considered to be a hallmark of PD. However, the exact changes in native ⍺-synuclein protein species after exercise and the downstream effects of exercise upon the health of the animals remains unclear. Recently, it was shown that swimming constitutes a form of exercise in C. elegans worms that confers a protective effect in several worm models of tau and Huntington protein neurodegeneration. Here we show that a period of swimming exercise (Ex) — 15-20 mins — dramatically reduces several native human ⍺-synuclein protein species in the NL5901 C. elegans worm model of Parkinson’s. Exercise on Day 1 of adulthood was found to improve motor function measured by the thrashing rate of worms on Day 2 and Day 4 when compared to both control (untreated) and food restricted (FR) worms. Moreover, exercised worms show smaller ⍺-synuclein::YFP puncta than food restricted worms. Here we show that exercise reduces native human ⍺-synuclein levels independent of food restriction in C. elegans.