Health
Exercise in gene therapy reverses the malaise of mice with common myotonic dystrophy
Adding exercise to the gene therapy for myotonic dystrophy type 1 (DM1) was more effective in reversing malaise than treatment alone in a study using a mouse model of the disease. In fact, exercise alone had some effect, but gene therapy alone had no effect. Conducted by researchers and collaborators at Massachusetts General Hospital (MGH), the study affects patients experiencing fatigue from genetics-related musculoskeletal disorders and fatigue from other types of illnesses. Give.The study will be displayed in Molecular Therapy-Nucleic Acid..
It is encouraging that exercise makes a significant difference on its own, and in combination with gene therapy tailored specifically for the disease. “
Thurman M. Wheeler, MD, Investigator, Department of Neurology at MGH and Harvard Medical School
Wheeler was the senior author of this study.
DM1 is the most common muscular dystrophy in adults and is one of several genetic conditions that cause muscle wasting and progressive weakness. Patients with DM1 report that chronic fatigue is the most debilitating symptom of their condition, but the biological basis for this effect is unknown. Wheeler and his colleagues wanted to test the value of exercise to reverse this condition.
The disease is caused by gain-of-function mutations that lead to the expression of high levels of genetic elements called extended microsatellite CUG repeats. Researchers used mice genetically engineered to have the same defects and treated some of them with antisense oligonucleotides. Antisense oligonucleotides are strands of genetic material that attach to RNA to repair specific genetic defects.
Next, aged mice with a gene defect that received only oligonucleotides, those who were forced to exercise only, those who received both treatment and exercise, and the effects of exercise on the placebo (saline) -treated group I studied. They compared post-exercise activity levels of mice in each of these groups in the study. They also measured the response of defective young mice that had just been treated with placebo. Mouse activity was measured using a special type of enclosure that records mouse movements.
This study provides preliminary answers to at least two questions. How effective should scientists be in gene therapy for this disease in real-world patients? And can exercise benefit such patients?
“By itself, I was surprised that exercise helped the mice recover from exercise faster,” Wheeler says. “Exercise and antisense therapy were even more effective, but antisense alone had no measurable benefit.”
While it seems common sense that exercise helps patients suffering from weakness, some clinicians and researchers wonder if exercise can have the opposite effect and actually accelerate patient decline. I thought. Studies by Wheeler and his colleagues have instead suggested that the effects of exercise may be beneficial to these patients and other patients with similar conditions.
Source:
Journal reference:
Hu, N. , et al. (2020) Antisense oligonucleotides and adjuvants Exercise therapy reverses malaise in aged mice with myotonic dystrophy. Molecular therapy: Nucleic acid. doi.org/10.1016/j.omtn.2020.11.014..
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