Regular exercise prevents the degradation of neurons vital for movement in rats with symptoms of Parkinson’s disease, emphasising the importance of physical activity in the condition. The finding could also lead to new treatments for the disease.
Parkinson’s disease is a neurodegenerative disorder caused by a loss of dopamine-producing neurons in the substantia nigra, an area of the brain involved in movement. This can lead to tremors, loss of motor control, impaired balance or speech and other symptoms.
Previous research has shown intense exercise can slow the progression of early-stage Parkinson’s disease. To understand why, Paolo Calabresi at the Catholic University of the Sacred Heart in Italy and his colleagues analysed the effect of physical activity on the brains of rats with symptoms of Parkinson’s.
They injected abnormal protein strands characteristic of Parkinson’s disease into the striatum, a brain region crucial for movement, in 19 rats. Of these rats, 13 exercised on a treadmill for 30 minutes daily, five days a week for a month. The rest remained sedentary.
After euthanising the animals, the team bathed slices of their brains in a solution that binds to a marker of dopamine, causing it to fluoresce. The sedentary rats had half as many dopamine-producing neurons in the substantia nigra, on average, as the active rats. This indicates that exercise may protect these cells from the harmful effects of the abnormal proteins.
Additional analysis revealed that neurons in the striata of active rats maintained the ability to strengthen connections with other cells – a trait critical for relaying motor signals – whereas this characteristic was impaired in sedentary rats. The researchers say this may be because exercise increased levels of certain proteins in the animals’ brains, such as brain-derived neurotrophic factor (BDNF), which helps neuron survive and grow.
Currently, no approved treatments curb the progression of Parkinson’s disease, says Calabresi. These findings suggest regular exercise may be one way of doing so, he says.
The work could also lead to the development of new drugs for the disease. “Once you know the molecular pathways that are being induced by exercise, you could conceive of having drugs that simulate those effects,” says David Eidelberg at the Feinstein Institutes for Medical Research in New York. This would be particularly beneficial for people with Parkinson’s who cannot intensely exercise.
However, this research may not translate to humans, especially given it only looked at one aspect of Parkinson’s disease pathology – the abnormal protein strands. It is unclear what role these play in the disease, says Eidelberg. In fact, some people with Parkinson’s don’t have them at all, he says.