The neuroprotective effects of exercise in multiple sclerosis (MS) may be assisted by the hormone irisin.
Studies have shown that irisin reduces nerve cell loss and alleviates clinical symptoms in mouse models of the disease, potentially making this hormone a new therapeutic target. And unlike existing MS treatments that target the immune system, it is thought to work by strengthening protective genetic programs within the nerve cells themselves, suggesting a new approach to halting MS neurodegeneration.
“We are optimistic that our study will open up further development of irisin, particularly as a treatment for progressive MS,” Christiane D. Lunn, Ph.D., a neuroscientist and principal investigator at the Massachusetts General Brigham Neuroscience Institute and McCance Center for Brain Health, said in the institute’s press release. “Our findings strengthen the argument that irisin may help protect neurons in multiple types of neurodegenerative diseases.”
A study found that the exercise hormone irisin has neuroprotective effects in a mouse model of multiple sclerosis. natural metabolism.
Aerobic exercise is considered a potential disease-modifying intervention in MS because it can improve physical fitness and slow the progression of neurological symptoms. However, the exact biological mechanisms are unknown and there are no existing drugs that can reproduce these effects.
Benefits of irisin
Irisin has emerged as a promising candidate that may mediate some of the neuroprotective effects of exercise. Research has shown that exercise increases the activity of the gene encoding the irisin precursor protein in skeletal muscle and brain, which increases irisin levels in the blood.
Wrann et al. previously showed that irisin can improve cognitive function and reduce neuroinflammation in a mouse model of Alzheimer’s disease. A similar study demonstrated the benefits of irisin in a mouse model of Parkinson’s disease.
The research team set out to investigate the effects of irisin on the progression of MS in mice suffering from experimental autoimmune encephalomyelitis, an induced disease commonly used to model MS.
Some animals were given free access to a running wheel for 8 weeks before MS induction, whereas others were not given access to a functional running wheel.
After MS induction, mice that performed spontaneous freewheel running exercise recovered faster from peak symptoms and had less neuronal loss in the spinal cord. And the gene encoding the precursor protein for irisin was significantly increased in the calf muscles of running mice.
When the same protocol was applied to mice lacking the irisin gene, the exercised animals showed no improvement in MS symptoms or reduced neuronal loss compared to sedentary mice. The findings suggest that “irisin is required for the neuroprotective effects of voluntary running.” [MS] model,” the team wrote.
To test whether irisin-based therapy can prevent neurodegeneration, we injected mice with a viral vector carrying the irisin gene on the day of MS induction. This improved recovery from peak MS symptoms, reduced neuron loss in the spinal cord, and reduced immune cell infiltration.
Control MS mice lost the ability to distinguish between different environments in a memory test, but irisin treatment restored this ability. Irisin treatment also reduced neuron loss in the hippocampus, a brain region involved in memory.
Additional experiments showed that the neuroprotective effects of irisin in MS are mediated not by changes in immune responses, but by activation of neural genes involved in neuroprotection.
“We did not find a direct suppressive effect of irisin on peripheral immunity, but rather a direct neuroprotective effect,” said Ruxandra F. Silbulescu, Ph.D., co-senior author of the study and a neuroimmunologist at the Massachusetts General Brigham Neuroscience Institute.
Imaging studies of MS spinal cord tissue detected loss of synapses, the junctions where neurons communicate with each other. However, this loss was reversed in both irisin-treated mice and MS mice that performed spontaneous running. The function of mitochondria, the cells’ energy producers, also improved in treated and running mice.
The researchers then confirmed that irisin binds directly to motor neurons in the spinal cord.
“What we found particularly interesting is that exercise-induced molecules can directly protect neurons in a mouse model of multiple sclerosis. This reveals a fundamentally new mechanism by which exercise influences neurodegeneration in MS,” said Sheena C. Rosenkranz, MD, lead author of the study and head of the Behavioral Intervention Group at the Institute of Neuroimmunology and Multiple Sclerosis at the University Medical Center Hamburg-Eppendorf.
“Our results using irisin in a treatment regimen strongly support irisin as an attractive drug target to counter neurodegeneration in the advanced stages of MS, pending validation in future studies,” the research team concluded.
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