Stanford scientists discover fountain of youth molecule that revives deteriorating muscles - now the

Stanford scientists have discovered a molecule they hope could be turned into an anti-aging drug.

Testing in lab mice revealed that by blocking the action of an aging-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 wide-reaching implications for adults who start seeing muscle strength wane 10 percent with every passing decade, as well as tens of thousands of Americans with muscle-wasting diseases such as amyotrophic lateral sclerosis (ALS).

Old mice that had endured damage to their sciatic nerve were administered shots of the molecule daily for a month. Stanford researchers found that by inhibiting 15-PGDH, they were able to restore PGE2 to levels typically found in younger mice and their muscle fibers grew back larger and stronger

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 to regenerate muscle while boosting levels of a replenishing molecule called prostaglandin E2 (PGE2). 

The Stanford University research team’s latest finding expands on earlier research that showed blocking 15-PGDH, also known as a gerozyme, significantly improved the mice’s leg strength and endurance when running on a treadmill.

Dr Helen Blau, the lead researcher, and director of the Baxter Laboratory for Stem Cell Biology at Stanford University, said: ‘This is the first time a drug treatment has been shown to affect both muscle fibers and the motor neurons that stimulate them to contract in order to speed healing and restore strength and muscle mass. It’s unique.

‘PGE2 is part of the body’s natural healing mechanism, and its levels increase in muscle after injury. We wanted to learn how age triggers an increase in 15-PGDH, and therefore the degradation and loss of PGE2.’

In 2021, the research team began daily injections of a small 15-PGDH-blocking molecule into 24-month-old mice, which is technically old age for the animals. They simulated an injury to the mice’s sciatic nerves before administering the treatments.

They found that inhibiting 15-PGDH even partially restored PGE2 to levels typically found in younger mice and their muscle fibers grew back larger and stronger.

They now know why this is. 15-PGDH builds up in muscles while breaking down PGE2 as people age.

PGE2 is released by the body in response to inflammation such as a muscle tear or strain in order to speed up the healing process.

The researchers also identified hidden clumps of 15-PGDH in the muscle fibers of people with neuromuscular disorders such as ALS, muscular dystrophy, and multiple sclerosis, suggesting that the gerozyme may have a role in causing these debilitating human disorders.

Dr Blau said: ‘Our next steps will be to examine whether blocking 15-PGDH function in people with spinal muscular atrophy can increase lost muscle strength in combination with gene therapy or other treatments.

‘We are also looking at ALS to see if something like this might help these patients. It’s really exciting that we are able to affect both muscle function and motor neuron growth.’

Muscle frailty is especially common in seniors, affecting around 30 percent of people over 80. But the course of muscle deterioration starts as early as one’s 50s.

It also has a steep economic cost. As muscles waste away over time, a person loses their ability to work and care for themselves, have a higher risk of a bad fall or other injury, and become increasingly less mobile.

The result is billions spent by the government to care for seniors at greatest risk of harm, on top of the mountain of money spent by insurance companies to cover the cost of care for the millions who don’t get coverage through the federal government.

The study is published in the journal Science Translational Medicine.

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