New Study Reveals Exercise’s Therapeutic Effects on Parkinson’s Disease
A new study conducted by a group of neuroscientists from the Faculty of Medicine of the Catholic University and the Gemelli Foundation in Rome sheds light on the physiological mechanisms behind the therapeutic effects of intense physical exercise on Parkinson’s disease. The findings, published in Science Advances, suggest that exercise performed in the early stages of the disease can lead to long-lasting improvements in motor and cognitive symptoms.
Previous research has already established the positive effects of regular aerobic activity on Parkinson’s disease. However, this Italian study has uncovered a biological mechanism previously unknown. “We have discovered a biological mechanism never observed before, through which exercise performed in the early stages of the disease induces beneficial effects on movement control that can persist over time even after the suspension of training,” explains lead author Professor Paolo Calabresi.
One important factor identified by the study is the increased production of brain neutrophic factor (BDNF) associated with intense physical activity. BDNF is a protein that promotes the formation of new neurons and synapses while providing neuroprotective effects. Interestingly, the research suggests that certain activities, such as swimming, running, and cycling, stimulate nerve cell production more effectively than anaerobic exercises like weightlifting.
To investigate the impact of exercise on Parkinson’s disease, the scientists conducted experiments on mice with the disease. The mice were put through daily treadmill exercises for one month, and the results were promising. The exercise led to increased production of BDNF in the brains of the mice, contributing to the slowing down of the disease’s progression. Notably, there was a reduction in the diffusion of toxic aggregates of a protein called alpha-synuclein, which is known to cause the degeneration of nerve cells implicated in motor control.
The neuroprotective impact of exercise is attributed to its ability to preserve dopamine-producing neurons and maintain their proper functioning, both of which are compromised by Parkinson’s disease. The study also revealed that BDNF interacts with the NMDA glutamate receptor, allowing neurons in the striatum to respond effectively to stimuli. These effects were observed to last beyond the exercise period, highlighting the long-term benefits of physical activity on the brain.
Building on these findings, Professor Calabresi and his team are now conducting a clinical study to explore whether intensive exercise can help identify new markers for monitoring disease progression in early-stage patients. The study will also investigate the involvement of glial cells, specialized cells that provide support to neurons, to better understand the underlying molecular and cellular mechanisms behind the observed positive effects of exercise.
These discoveries open up new possibilities for developing targeted exercise interventions tailored to individuals with Parkinson’s disease. With further research and understanding, exercise could become an integral part of the treatment and management of this debilitating condition, offering hope for improved quality of life for patients worldwide.