- Mice that received the injections saw muscles regenerate larger and stronger
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Stanford scientists have discovered a molecule that they hope could be turned into an anti-aging drug.
Tests on laboratory mice found that by blocking the action of an age-related protein in the body called 15-PGDH, they could repair broken nerve and muscle fiber connections to restore strength and muscle mass.
The discovery could have far-reaching implications for adults, whose muscle strength is declining by 10 percent every decade, as well as tens of thousands of Americans with muscle-wasting diseases such as amyotrophic lateral sclerosis (ALS).
Old mice whose sciatic nerves were damaged were given daily injections of the molecule for a month. Stanford researchers found that by inhibiting 15-PGDH, they were able to restore the levels of PGE2 typically found in younger mice and their muscle fibers became larger and stronger again
Their research is the first to show that damaged motor neurons in the brain and spinal cord can be regenerated by blocking the activity of 15-PGDH for muscle regeneration while increasing levels of a regenerating molecule called prostaglandin E2 (PGE2).
The latest findings from the Stanford University research team expand on previous research It was found that blocking 15-PGDH, also known as gerozyme, significantly improved the mice’s leg strength and endurance when running on a treadmill.
Dr. Helen Blau, principal investigator and director of the Baxter Laboratory for Stem Cell Biology at Stanford University, said: “This is the first time that drug treatment affects both the muscle fibers and the motor neurons that stimulate them to contract to accelerate healing and restore strength and muscle mass.” It is unique.
“PGE2 is part of the body’s natural healing mechanism and its levels in muscle increase after an injury.” “We wanted to find out how age triggers an increase in 15-PGDH and thus the degradation and loss of PGE2.”
In 2021, the research team began daily injecting a small 15-PGDH-blocking molecule into 24-month-old mice, which is technically the age of the animals. They simulated injury to the mice’s sciatic nerves before administering the treatments.
They found that inhibiting 15-PGDH even partially restored PGE2 to levels typical in younger mice, and their muscle fibers became larger and stronger again.
Now you know why that is. 15-PGDH builds up in muscles while PGE2 breaks down as we age.
PGE2 is released by the body in response to inflammation, such as a muscle tear or strain, to speed up the healing process.
The researchers also identified hidden clumps of 15-PGDH in the muscle fibers of people with neuromuscular diseases such as ALS, muscular dystrophy and multiple sclerosis, suggesting that the gerozyme may play a role in the development of these debilitating human diseases.
Dr. Blau said: “Our next steps will be to study whether blocking 15-PGDH function in people with spinal muscular atrophy can increase muscle strength loss in combination with gene therapy or other treatments.”
“We’re also looking at ALS to see if something like this could help these patients.” “It’s really exciting that we can influence both muscle function and motor neuron growth.”
Muscle weakness is particularly common in seniors and affects around 30 percent of people over 80. However, the process of muscle loss begins in the 50s.
It also has a high economic cost. As muscles atrophy over time, a person loses their ability to work and care for themselves, is at greater risk of a serious fall or other injury, and becomes less and less mobile.
The result is billions that the government spends on caring for seniors who are most at risk, in addition to the piles of money that insurance companies spend to cover the cost of care for the millions who do not receive coverage from the federal government.
The study is published in the journal Scientific translational medicine.