- Parkinson’s disease is a progressive neurodegenerative condition that affects more than 8.5 million people worldwide.
- Symptoms, such as tremors, muscle stiffness, slowness of movement, and cognitive decline, gradually worsen over time.
- Some medications can relieve symptoms and improve quality of life, but there is currently no cure.
- New research has found that a hormone produced during exercise reduces levels of the protein responsible for Parkinson’s symptoms.
- The finding in mice may point to new treatments for the disease.
According to the World Health Organization (WHO), Parkinson’s disease (PD), a degenerative condition of the brain, is increasing faster than any other neurological disorder. Worldwide, the prevalence has doubled in the last 25 years.
Parkinson’s symptoms develop slowly, getting worse over time, and may include the following:
- tremors
- Impaired coordination and balance.
- a loss of the sense of smell
- gait changes
- changes in the nerves that control the muscles of the face
- trouble sleeping
- mood swings, including depression
- fatigue
There is currently no cure for the disease, although medications, occupational therapy, speech therapy, and exercise can relieve symptoms.
Many of the symptoms May be due to the accumulation of alpha-synuclein lumps, leading to the death of brain cells. A new study in mice, published in PNASdiscovered that a hormone produced during aerobic exercise can prevent these lumps from forming.
“The results of this study are significant because, although we know that physical activity and exercise are beneficial for people with Parkinson’s, it is currently unclear how this affects the cells and processes in the brain that contribute to symptoms of the disease. . This study sheds some light on how a hormone produced during exercise might be acting to protect vital brain cells from dying in Parkinson’s disease.”
– Dr. Katherine Fletcher, Research Communications Manager at Parkinson’s UK.
Studies have shown that exercise can improve cognitive function and benefit people with Parkinson’s or Alzheimer’s. Recent research identified irisina molecule secreted into the blood during endurance exercise, which may contribute to this benefit.
Because irisin is secreted in the same way in humans and mice, researchers at Johns Hopkins Medicine and the Dana-Farber Cancer Institute in Boston created a mouse model of Parkinson’s to investigate it further.
First, the researchers engineered mouse brain cells to produce alpha-synuclein fibers. When this protein forms clumps, like those found in the brains of people with PD, the clumps kill dopamine producers. neurons.
The researchers administered irisin to these nerve cells in vitro and found that alpha-synuclein fibers did not form clumps. Irisin also prevented brain cells from dying.
After success in vitro, the researchers moved on to experiments in live mice designed to have Parkinson-like symptoms.
First, they injected alpha-synuclein into an area of the mouse brain called striatum, which has many dopamine-producing neurons. Two weeks later, they injected irisin into the mice’s tail vein.
After 6 months, the mice that were not injected with irisin showed muscle deterioration. They had reduced grip strength and were less able to get down a pole.
The mice that had received the irisin had no muscle movement deficits.
The researchers found that irisin given by injection had crossed the blood brain barrier and blocked the formation of alpha-synuclein clumps. Essentially, irisin had no effect on alpha-synuclein monomers thought to be important in transmit nerve impulses.
When the researchers analyzed the brain tissue of the mice, they found that accumulations of alpha-synuclein were reduced by up to 80% in the mice that received irisin, compared to those that received placebos.
Further investigation showed that this effect was due to lysosomal degradation from the alpha-synuclein groups, which the researchers suggest was promoted by irisin.
They state, “Our demonstration that irisin reduces pathologic α-syn is particularly relevant to the pathogenesis of PD and related α-synucleinopathies, as pathologic α-syn appears to be the primary pathogenetic driver of these disorders.”
“Since irisin is a naturally occurring peptide hormone and appears to have evolved to cross the blood-brain barrier, we believe irisin is worth further evaluation as a potential therapy for Parkinson’s and other forms of neurodegeneration,” said the corresponding author. Dr Bruce Spiegelman, Ph.D. from the Dana-Farber Cancer Institute.
Although this study was conducted on mice, irisin is also secreted from the muscle and skeletal tissues of people during exercise. However, exercise alone may not produce sufficient amounts to have these effects, as noted by Dr. Fletcher:
“It is not clear from these results whether exercise alone would generate enough irisin to have protective effects or whether using other means of stimulating this hormone might be a more realistic therapeutic option in the future.”
The finding that injected irisin can cross the blood-brain barrier to reach alpha-synuclein groups may therefore hold the key to its potential use as a treatment for Parkinson’s disease.
The researchers acknowledge that their findings are an initial step in the search for an effective treatment for Parkinson’s disease, but they are optimistic about its potential.
“There is considerable promise that it could be developed as a disease-modifying therapy for the treatment of PD. […] It will be important for any future human therapy to determine whether irisin can stop the progression of experimental PD after neurological symptoms have begun and to determine the effects of irisin in other models of PD.”
While welcoming the research, Dr. Fletcher emphasized the need for further study: “Until now, the research has been done in a laboratory setting and will need further development before paving the way for a future therapy that could slow or stop the condition for people with Parkinson’s.”
However, he added: “Anything that shows promise in protecting brain cells in Parkinson’s offers hope, as there are currently no treatments that can slow or stop the disease.”
