How to Reverse Muscle Loss Due to Aging

An international team led by uOttawa Faculty of Medicine researchers have published findings that could contribute to future therapeutics for muscle degeneration due to old age, and diseases such as cancer and muscular dystrophyIn a study appearing in the Journal of Cell Biology, which publishes peer-reviewed research on cellular structure and function, the authors said their work demonstrates the importance of the enzyme GCN5 in maintaining the expression of key structural proteins in skeletal muscle. Those are the muscles attached to bone that breathing, posture and locomotion all rely on.

We found that if you delete GCN5 expression from muscle it will no longer be able to handle extreme physical stress,” says Dr. Keir Menzies, a molecular biologist at the Faculty of Medicine’s Biochemistry, Microbiology and Immunology department and cross-appointed as an associate professor at the Interdisciplinary School of Health Sciences.

Over the span of roughly five years, the uOttawa-led international collaboration painstakingly experimented with a muscle-specific mouse knockout” of GCN5, a well-studied enzyme which regulates multiple cellular processes such as metabolism and inflammation. Through a series of manipulations, scientists produce lab mice in which specific genes are disrupted, or knocked out, to unveil animal models of human disease and better understand how genes work.

In this case, multiple experiments were done to examine the role the GCN5 enzyme plays in muscle fiber. What they found with this line of muscle-specific mouse knockouts was a notable decline in muscle health during physical stress, such as downhill treadmill running, a type of exercise known by athletes to cause micro-tears in muscle fibres to stimulate muscle growth. The lab animals’ muscle fibers became dramatically weaker as they scurried downhill, like those of old mice, while wild-type mice were not similarly impacted

Dr. Menzies, the senior author of the study, says the findings are akin to what is observed in advanced aging, or myopathies and muscular dystrophy, a group of genetic diseases that result in progressive weakness and loss of muscle mass. It was supported by human data, including an observed negative correlation between muscle fiber diameter and Yin Yang 1, a highly multifunctional protein that is pivotal to a slew of cellular processes and found by the Menzies lab to be a target of GCN5. Ultimately, the team’s research found that GCN5 boosts the expression of key structural muscle proteins, notably dystrophin, and a lack of it will reduce them.

Source: https://rupress.org/
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https://www.thebrighterside.news

COVID-19 Can Cause Antibodies that Mistakenly Target your Own Tissues

An increasing body of research is pointing toward the possibility that COVID-19 causes the development of autoantibodies linked to other autoimmune diseases — and may be tied to the long-hauler symptoms associated with coronavirus.

In the latest preprint study (which means it has not yet undergone peer review) researchers analyzed the levels of 18 different autoantibodies between four groups:

  • 29 unexposed pre-pandemic individuals from the general population
  • 20 individuals hospitalized with moderate-to-severe COVID-19
  • 9 recovering COVID-19-infected individuals with asymptomatic to mild viral symptoms during the acute phase, with samples collected between 1.8 and 7.3 months after infection
  • 6 unexposed pre-pandemic subjects with lupus (an autoimmune disease that involves different kinds of autoantibodies)
  • Autoantibodies are antibodies that mistakenly target your own tissues or organs and are associated with diseases such as rheumatoid arthritis and lupus. Unsurprisingly, the researchers found that autoantibodies were detected in five out of the six lupus subjects, compared to just 11 of 29 non-lupus, pre-pandemic controls.

However, the researchers also found that autoantibodies were detected in seven out of nine patients recovering from SARS-CoV-2 and in 12 out of the 20 hospitalized individuals with moderate to severe COVID-19. In the first group, autoantibodies were detected in all patients with reported persistent symptoms and two of the four without any long-term symptoms.

The autoantibodies that set SARS-CoV-2  infected patients apart from the pre-pandemic subjects are widely associated with myopathies (neuromuscular disorders), vasculitis (inflammation of the blood vessels), and antiphospholipid syndromes (when your body creates antibodies that make your blood much more likely to clot), all of which are conditions that share some similarities with COVID-19. The researchers note that these results underscore the importance of further investigating autoimmunity during a COVID-19 infection, and the role of autoimmunity in lingering symptoms. That said, they do urge caution in interpreting the results, which still need to undergo peer review.

It’s a signal; it is not definitive,” lead researcher Nahid Bhadelia, MD, told the New York Times. We don’t know how prevalent it is, and whether or not it can be linked to long COVID.” (Long COVID is sometimes used to describe the syndrome that causes long-hauler symptoms in those who have recovered from COVID-19.)

Still, as many as one-third of COVID-19 survivors say they still experience symptoms — and determining the role autoimmunity may play after coronavirus infection is critical.

This is a real phenomenon,” Dr. Bhadelia said. “We’re looking at a second pandemic of people with ongoing potential disability who may not be able to return to work, and that’s a huge impact on the health symptoms.”

Source: https://creakyjoints.org/
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https://www.medrxiv.org/