Neurorestoration by physical exercise: moving forward

Abstract

Although a good deal is known about the pathophysiology of Parkinson's disease and information is emerging about its cause, there are no pharmacological treatments shown to have a significant, sustained capacity to prevent or attenuate the condition. However, accumulating clinical evidence suggests that physical exercise can provide this much needed treatment, and studies of animal models of the dopamine deficiency associated with the motor symptoms of Parkinson's disease further support this hypothesis. Thus, in our collaborative research efforts, we seek to understand the biological basis for exercise-induced protection in order to assist in the development of a safe and clinically effective intervention based on increased physical activity. In addition, we recognize that some individuals cannot or will not engage in physical exercise, and believe that mechanistic studies of exercise-induced protection will provide insights into the development of drugs that could emulate its effects. Using toxins that induce a deficiency of dopamine, we have affirmed that physical exercise can reduce behavioral and neurobiological deficits induced by such toxins, and suggest that these neuroprotective effects are likely to involve the activation of signaling cascades by neurotrophic factors such as glial cell line derived neurotrophic factor.