Parkinson’s disease: exercise can stop the degradation of crucial neurons – New Scientist

Regular exercise prevents the breakdown of neurons vital for movement in rats with symptoms of Parkinson’s disease, highlighting the importance of physical activity in the condition. The finding may 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 that vigorous exercise can slow the progression of early-stage Parkinson’s disease. To understand why, Paolo Calabresi of 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 brain region critical 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 the animals were euthanized, 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, on average, half as many dopamine-producing neurons in the substantia nigra as the active rats. This indicates that exercise can protect these cells from the harmful effects of the abnormal proteins.

Additional analysis revealed that neurons in the striata of active rats retained the ability to strengthen connections with other cells – a property critical for motor signal transmission – while this characteristic was reduced 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 treatments slow the progression of Parkinson’s disease, Calabresi says. These findings suggest that regular exercise may be one way to do this, he says.

The work could also lead to the development of new drugs for the disease. “Once you know the molecular pathways caused by exercise, you can imagine having drugs that simulate those effects,” says David Eidelberg of the Feinstein Institutes for Medical Research in New York. This would be particularly beneficial for people with Parkinson’s who cannot exercise vigorously.

However, this research may not translate to humans, especially since it only looked at one aspect of Parkinson’s disease pathology: the abnormal protein strands. It’s 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.

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