A protein that causes Parkinson’s symptoms can have its levels lowered by an exercise-induced hormone.
- Over 8.5 million individuals worldwide are afflicted with the progressive neurological disorder known as Parkinson’s disease.
- Tremors, stiffness in the muscles, sluggish movement, and cognitive decline are some of the symptoms that progressively get worse over time.
- Although there is no cure at this time, several drugs help reduce symptoms and enhance the quality of life.
- A hormone released during exercise lowers the amounts of protein that cause the symptoms of Parkinson’s disease, according to recent research.
- The results in mice might lead to the development of novel disease-modifying therapies.
More people are being diagnosed with Parkinson’s disease (PD), a brain ailment that is deteriorating. In the previous 25 years, the prevalence has increased by a factor of two globally.
Parkinson’s disease symptoms might include the following and usually start out mildly before getting worse with time:
- decreased balance and coordination issue
- a decline in smell sensibility
- the nerves that govern the face muscles undergo alterations
- trouble sleeping
- sadness and other variations in mood
Although, drugs, occupational therapy, speech therapy, and exercise helps lessen the symptoms as there is presently no cure for the condition.
The aggregation of alpha-synuclein clumps, which cause the death of brain cells, maybe the cause of many of the symptoms.
Exercise may aid patients with Parkinson’s or Alzheimer’s disease and enhance cognitive function, according to studies. Irisin, a chemical produced in the blood during endurance exercise, has been found to perhaps contribute to this advantage, according to recent studies.
Since irisin is secreted in the same manner in both people and animals, scientists from Johns Hopkins Medicine and the Dana-Farber Cancer Institute in Boston developed a Parkinson’s disease mouse model to continue their research.
The scientists first produced alpha-synuclein fibers in mouse brain cells using genetic engineering. Dopamine-producing neurons are killed by these protein clumps when they develop, as shown in the brains of PD patients.
After giving these nerve cells irisin in vitro, the researchers discovered that the alpha-synuclein fibers did not group together. The death of the brain cells was also stopped by the irisin.
Result of muscle action
Following their in vitro success, the researchers turned to trials using live mice that had been modified to exhibit symptoms similar to those of Parkinson’s disease.
They started by injecting alpha-synuclein into the striatum, a region of the mouse brain with a large number of dopamine-producing neurons. They gave the mice an injection of irisin into their tail veins two weeks later.
Mice that had not received irisin injections after six months displayed weakened muscles. They were less able to descend a pole and had weaker grips.
The irisin-treated mice showed no impairments in their ability to move their muscles.
The scientists discovered that intravenous irisin had successfully penetrated the blood-brain barrier and prevented the production of alpha-synuclein aggregates. The most significant finding was that irisin had no effect on alpha-synuclein monomers, which are believed to be crucial for sending nerve impulses.
The brain changes
When scientists examined the mice’s brain tissue, they discovered that animals administered irisin had lower levels of alpha-synuclein aggregates than mice given placebos—up to 80% lower.
Further study revealed that the cause of this impact was the lysosomal breakdown of the alpha-synuclein clumps, which the researchers hypothesize was aided by irisin.
Since pathologic -syn appears to be the primary pathogenic driver of these illnesses, they claim that “our finding that irisin lowers pathologic -syn is particularly important to the etiology of PD and similar -synucleinopathies.”
Potential therapies for Parkinson’s
We believe it is worthwhile to keep assessing irisin as a possible treatment for Parkinson’s and other types of neurodegeneration given that it is a naturally occurring peptide hormone and appears to have evolved to penetrate the blood-brain barrier.
Despite the fact that this work was done on mice, skeletal and muscular tissues in humans also release irisin when they exercise. Exercise by itself, though, might not generate enough of these things to have these benefits.
These findings make it difficult to determine whether exercise alone would produce enough irisin to have protective benefits or whether alternative strategies for increasing this hormone would represent a more practical treatment approach in the future.
Its potential application as a therapy for Parkinson’s disease may thus depend on the discovery that injected irisin may pass the blood-brain barrier and reach the alpha-synuclein clumps.
The first stage in the hunt for PD cures
The researchers are upbeat about the possibility of their results despite the fact that they recognize that they are just the first step in the search for a successful Parkinson’s disease treatment.
The potential for its development as a disease-modifying medication for the treatment of Parkinson’s disease is quite promising. It will be crucial to ascertain if irisin can stop the advancement of experimental PD after neurological symptoms have begun, as well as the effects of irisin in additional PD models before any further human treatments are implemented.
Before opening the way for a future therapy that could be able to slow down or halt the condition of people with Parkinson’s, the study, which has thus far been conducted in a lab environment, will need to be further developed.
There is presently no known medication that may prevent or reduce the progression of Parkinson’s disease, therefore anything that shows promise in preserving brain cells in this disease gives hope.