Abstract
Parkinson's disease (PD) is manifested by progressive motor, autonomic, and cognitive disturbances. Dopamine (DA) synthesizing neurons in the substantia nigra (SN) degenerate, causing a decline in DA level in the striatum that leads to the characteristic movement disorders. A disease-modifying therapy to arrest PD progression remains unattainable with current pharmacotherapies, most of which cause severe side effects and lose their efficacy with time. For this reason, there is a need to seek new therapies supporting the pharmacological treatment of PD. Motor therapy is recommended for pharmacologically treated PD patients as it alleviates the symptoms. Molecular mechanisms behind the beneficial effects of motor therapy are unknown, nor is it known whether such therapy may be neuroprotective in PD patients. Due to obvious limitations, human studies are unlikely to answer these questions; therefore, the use of animal models of PD seems indispensable. Motor therapy in animal models of PD characterized by the loss of dopaminergic neurons has neuroprotective and neuroregenerative effects, and the completeness of neuronal protection may depend on (i) degree of neuronal loss, (ii) duration and intensity of exercise, and (iii) time elapsed between insult and commencing of training. As the physical activity is neuroprotective for dopaminergic neurons, the question arises what is the mechanism of this protective action. A current hypothesis assumes a central role of neurotrophic factors in the neuroprotection of dopaminergic neurons, even though it is still not clear whether increased DA level in the nigrostriatal axis results from neurogenesis of dopaminergic neurons in the SN, recovery of the phenotype of dopaminergic neurons, increased sprouting of the residual dopaminergic axons in the striatum, or generation of local striatal neurons from inhibitory interneurons. In the present review, we discuss studies describing the influence of physical exercise on the PD-like changes manifested in animal models of the disease and focus our interest on the current state of knowledge on the mechanism of neuroprotection induced by physical activity as a supportive therapy in PD.
Highlights
Parkinson’s disease (PD) is the second most common neurodegenerative disorder
We aimed to describe the influence of physical exercise on PD symptoms in animal models of the disease and report the current state of knowledge concerning the mechanism underlying the neuroprotective effects of physical activity as supportive therapy in PD
In our study [71], the results suggest that 10 weeks of training on the treadmill, no matter if started before or after PD induction, have a protective effect against dopaminergic neuron degeneration in the chronic MPTP mouse model of PD
Summary
Parkinson’s disease (PD) is the second most common neurodegenerative disorder. Due to the frequency of occurrence, it is a serious medical, social, and economic problem. Pharmacological therapy is the current gold standard in the treatment of PD, recent clinical trials have shown that physical activity alleviates and slows down the development of movement impairments, reduces depression and anxiety, and improves mood state, cognitive function, and sleep quality [1, 2]. Recent studies have shown that regular physical activity, such as strength training, walking, flexibility, balance, and aerobic training or dance, adjusted to the severity of the disease and to the current PD patient’s state of health, is able to enhance brain plasticity, which plays a key role in improving motor and cognitive functions [3]. We aimed to describe the influence of physical exercise on PD symptoms in animal models of the disease and report the current state of knowledge concerning the mechanism underlying the neuroprotective effects of physical activity as supportive therapy in PD. At present, despite the known ability of physical exercise to promote motoric improvement, our knowledge regarding the most beneficial form, duration, intensity, and frequency of exercise is still insufficient
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