Abstract
Epidemiological studies indicate that physical activity and exercise may reduce the risk of developing Parkinson's disease (PD), and clinical observations suggest that physical exercise can reduce the motor symptoms in PD patients. In experimental animals, a profound observation is that exercise of appropriate timing, duration, and intensity can reduce toxin-induced lesion of the nigrostriatal dopamine (DA) system in animal PD models, although negative results have also been reported, potentially due to inappropriate timing and intensity of the exercise regimen. Exercise may also minimize DA denervation-induced medium spiny neuron (MSN) dendritic atrophy and other abnormalities such as enlarged corticostriatal synapse and abnormal MSN excitability and spiking activity. Taken together, epidemiological studies, clinical observations, and animal research indicate that appropriately dosed physical activity and exercise may not only reduce the risk of developing PD in vulnerable populations but also benefit PD patients by potentially protecting the residual DA neurons or directly restoring the dysfunctional cortico-basal ganglia motor control circuit, and these benefits may be mediated by exercise-triggered production of endogenous neuroprotective molecules such as neurotrophic factors. Thus, exercise is a universally available, side effect-free medicine that should be prescribed to vulnerable populations as a preventive measure and to PD patients as a component of treatment. Future research needs to establish standardized exercise protocols that can reliably induce DA neuron protection, enabling the delineation of the underlying cellular and molecular mechanisms that in turn can maximize exercise-induced neuroprotection and neurorestoration in animal PD models and eventually in PD patients.
Highlights
Parkinson’s disease (PD) is a common, age-dependent degenerative neurological disorder caused by a severe loss of the nigrostriatal dopaminergic projection (Kish et al, 1988; Hornykiewicz, 2001; Braak et al, 2004; Kordower et al, 2013), leading to the characteristic motor deficits and symptoms including resting tremor, a slowness and paucity of movements, muscle rigidity, and posturalExercise-Induced Neuroprotection imbalance (Parkinson, 1817; Olanow et al, 2009)
Since the key pathology causing the motor deficits in PD patients and PD animal models is a severe loss of the nigrostriatal DA projection (Kish et al, 1988; Hornykiewicz, 2001; Franco and Turner, 2012; Li et al, 2015), an obvious important question is if the exercise-induced motor benefits in PD animal models and patients is at least partially mediated by a preservation or protection of residual nigrostriatal DA neurons, in addition to exercise’s beneficial effects directly on skeletal musculature
Many studies have been performed in animal PD models to investigate this question, starting with the publication of the study on the neuroprotective effect of forced limb use on DA neurons in a unilateral 6-OHDA rat PD model in 2001 (Tillerson et al, 2001)
Summary
Parkinson’s disease (PD) is a common, age-dependent degenerative neurological disorder caused by a severe loss of the nigrostriatal dopaminergic projection (Kish et al, 1988; Hornykiewicz, 2001; Braak et al, 2004; Kordower et al, 2013), leading to the characteristic motor deficits and symptoms including resting tremor, a slowness and paucity of movements, muscle rigidity, and postural. Physical exercise has been reported to produce synergistic benefits with L-dopa for improving motor functions in PD patients (Kang et al, 2012) Taken together, these clinical and epidemiological studies have provided evidence supporting the conclusion that exercise has a significant preventive effect on PD, and has therapeutic value by reducing the symptoms and slowing the symptom and disease progression (Figure 1), and should be promoted to the general population, PD vulnerable population in particular (Burley et al, 2016; Jackson et al, 2016; Lauzé et al, 2016). The forced use of the impaired limb is an excellent experimental design because the impaired limb was forced to performed natural motor activities that the limb was performing before the lesion; perhaps, more
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