Abstract

In “Long-term effect of regular physical activity and exercise habits in patients with early Parkinson disease,” Tsukita et al. reported that average regular physical activity levels over time were associated with slower deterioration of gait stability, activities of daily living, and processing speed in patients with Parkinson disease (PD). Darweesh et al. contextualized these findings by noting they are consistent with the results of other studies, suggesting that regular exercise may slow progression of PD. They further proposed that vigorous exercise may reduce the risk of PD, implying that the findings of Tsukita et al. may also be attributed to reverse causality. Tsukita et al. agreed that reverse causality is feasible, although other data suggest that exercise may change the brain, modifying the course of PD. However, Gupta questioned the pathophysiologic mechanism by which exercise changes the brain and affects disease progression in PD, commenting that perhaps motivation to exercise may be relevant to disease progression in PD. In light of these comments, Tsukita et al. reinforced the need for the following types of future research: (1) international, multicenter randomized controlled trials on the effect of exercise on disease progression (for patients with PD) and development of clinical symptoms of PD (for patients with prodromal PD) which include neuroimaging; (2) evaluation of the motivation for patients with PD to exercise; and (3) animal studies on the effect of exercise on the brain, which include neuropathology assessment of α-synuclein. In “Long-term effect of regular physical activity and exercise habits in patients with early Parkinson disease,” Tsukita et al. reported that average regular physical activity levels over time were associated with slower deterioration of gait stability, activities of daily living, and processing speed in patients with Parkinson disease (PD). Darweesh et al. contextualized these findings by noting they are consistent with the results of other studies, suggesting that regular exercise may slow progression of PD. They further proposed that vigorous exercise may reduce the risk of PD, implying that the findings of Tsukita et al. may also be attributed to reverse causality. Tsukita et al. agreed that reverse causality is feasible, although other data suggest that exercise may change the brain, modifying the course of PD. However, Gupta questioned the pathophysiologic mechanism by which exercise changes the brain and affects disease progression in PD, commenting that perhaps motivation to exercise may be relevant to disease progression in PD. In light of these comments, Tsukita et al. reinforced the need for the following types of future research: (1) international, multicenter randomized controlled trials on the effect of exercise on disease progression (for patients with PD) and development of clinical symptoms of PD (for patients with prodromal PD) which include neuroimaging; (2) evaluation of the motivation for patients with PD to exercise; and (3) animal studies on the effect of exercise on the brain, which include neuropathology assessment of α-synuclein.

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