Regular exercise prevents the degradation of neurons vital to movement in rats with symptoms of Parkinson’s disease, emphasizing 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 cause tremors, loss of motor control, impaired balance or speech, and other symptoms.
Previous research has shown that intense exercise can slow the early-stage Parkinson’s disease progression. To understand why, paolo calabresi at the Catholic University of the Sacred Heart in Italy and colleagues analyzed the effect of physical activity on the brains of rats with Parkinson’s symptoms.
They injected abnormal protein strands characteristic of Parkinson’s disease into the striatum, a region of the brain crucial for movement, in 19 rats. Of these rats, 13 exercised on a treadmill for 30 minutes a day, five days a week for one month. The rest remained sedentary.
After euthanizing the animals, the team bathed slices of their brains in a solution that binds to a dopamine marker, causing it to fluoresce. Sedentary rats had, on average, half as many dopamine-producing neurons in the substantia nigra as sedentary rats. active rats. This indicates that exercise may protect these cells from the deleterious effects of abnormal proteins.
Further analysis revealed that neurons in the striatum of active rats maintained the ability to strengthen connections with other cells, a critical trait for transmitting motor signals, whereas this trait 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 neurons survive and grow.
Currently, no approved treatment slows the progression of Parkinson’s disease, Calabresi says. These findings suggest that regular exercise may be one way to do it, she 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 envision having drugs that mimic those effects,” he says. david eidelberg at the Feinstein Institutes for Medical Research in New York. This would be particularly beneficial for people with Parkinson’s who are unable to exercise vigorously.
However, this research may not translate to humans, especially since it only looked at one aspect of Parkinson’s disease pathology: abnormal protein strands. It’s not clear what role these play in the disease, Eidelberg says. In fact, some people with Parkinson’s don’t have them at all, she says.
