US researchers have identified a protein responsible for causing fatigue in people with long Covid, Alzheimer’s and other diseases.
Representational Image [File photo]
US researchers have identified a protein responsible for causing fatigue in people with long Covid, Alzheimer’s and other diseases.
While infections and neurodegenerative diseases like Alzheimer’s are known to cause inflammation in the brain, the patients often develop muscle problems that seem to be independent of the central nervous system.
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A team led by the Washington University School of Medicine in St. Louis found that it is caused by a specific protein that travels from the brain to the muscles and leads to loss of muscle function.
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The study, conducted in fruit flies and mice, also identified ways to block this process. This may help physicians treat or prevent muscle wasting caused by bacterial infections, Alzheimer’s disease, and long Covid.
Aaron Johnson, Associate professor of developmental biology explained that when people are ill, “messenger proteins from the brain travel through the bloodstream and reduce energy levels in skeletal muscle.”
The “process reduces energy levels in skeletal muscle, decreasing the capacity to move and function normally”, he said, in the study, published in the journal Science Immunology.
For the study, the team modelled three different types of diseases — an E. coli bacterial infection, a SARS-CoV-2 viral infection, and Alzheimer’s.
They found that when the brain is exposed to inflammation, it builds up damaging chemicals called reactive oxygen species. This causes brain cells to produce an immune-related molecule called interleukin-6 (IL-6), which travels throughout the body via the bloodstream.
In mice, IL-6 was responsible — and the corresponding protein in fruit flies — for reducing energy production in muscles’ mitochondria, known as the cells’ energy factories.
They also found that IL-6 activates what is called the JAK-STAT pathway in muscle, and this is what causes the reduced energy production of mitochondria.
Currently, several therapeutics already approved by the Food and Drug Administration for other diseases can block this pathway, the team said.
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