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Stanford researchers have finally figured out how a therapy that blocks a single protein can reverse age-related muscle loss in mice — and the discovery suggests seniors might not be the only ones who could benefit from it.

Age-related muscle loss: People tend to start losing muscle mass and strength in their 30s, and from 50 on, you could be losing up to 10% of your muscle mass every decade.

While it is possible to regain lost muscle through exercise, health issues can make hitting the weights a challenge. If left unaddressed, though, age-related muscle loss can lead to decreased mobility and weakness, which increases the risk of falls or other injuries.

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Stem cell biologist Helen Blau of Stanford University School of Medicine and colleagues previously found that blocking 15-PGDH in old mice restored their withered muscles and improved their strength after a month of treatment. On the flip side, young mice lost muscle and became weaker after their levels of this enzyme were increased for a month.

Blau’s team has now found that 15-PGDH accumulates in the muscles of old mice as the connections that allow communication between muscles and nerves are lost, another consequence of aging. Treating old mice for one month with a drug that inhibits 15-PGDH restored these connections, called synapses, between muscle fibers and motor nerve cells, and boosted the animals’ strength, the team reports in the Oct. 11 Science Translational Medicine. Those synapses are how the brain directs muscles to move.

The findings suggest that blocking the gerozyme 15-PGDH may be a way to help recover strength that has diminished due to nerve injuries, motor nerve cell diseases or aging.

Looking for some good holiday reads? We’ve updated our list of best longevity books and added several from top longevity researchers like Dr. Harold Katcher, Dr. Morgan Levine, and Dr. Peter Attia.


Update 11/7/2023: This post has been updated since we originally published it in September 2020 and first updated it in April 2021. Several new best longevity books have been added to both the main list and honorable mentions sections, and the post has been cleaned up, and review ratings made current.

There are a lot of life extension and longevity books published every year.

A. Lot.

Researchers have uncovered that proteins use a common chemical label as a shield to protect them from degradation, which in turn affects motility and aging. Proteins are key to all processes in our cells and understanding their functions and regulation is of major importance.

“For many years, we have known that nearly all human proteins are modified by a specific chemical group, but its functional impact has remained undefined,” says professor Thomas Arnesen at the Department of Biomedicine, University of Bergen.

Aging is a natural process that affects all living organisms, prompting gradual changes in their behavior and abilities. Past studies have highlighted several physiological factors that can contribute to aging, including the body’s immune responses, an imbalance between the production of reactive oxygen (i.e., free radicals) and antioxidants, and sleep disturbances.

While the link between aging and these different factors is well-document, the connection between them is still poorly understood. Researchers at Washington University in St. Louis recently identified an immune molecule that could play a key role in modulating the process of aging and the duration living organism’s lifespan.

Their paper, published in Neuron, was inspired by two independent research efforts at the university.

Scientists from the University of California Davis (UC Davis) Comprehensive Cancer Center have recently published in Cell Death and Disease, identifying a critical protein that causes cells to die. The protein is described as an epitope, which is a section of the protein that is recognized by the immune system to activate a response. This epitope was distinctly found on the CD95 receptor, known to trigger programmed cell death. The report demonstrates a new mechanism to trigger cell death and provide further insight into improved disease treatments.

CD95 receptors, also referred to a “Fas”, are cell death receptors which are present on cell membranes. Once Fas is activated, it generates a signaling cascade which elicits cell death. The mechanism by which cells self-destruct has been an important research topic. By understanding cell death, scientists can generate better therapies for different diseases, including cancer.

Currently, cancer is treated by surgery, chemotherapy, or radiotherapy. Despite initial success, these treatments are unable to fully eradicate tumor cells. Immunotherapy is a new approach to target cancer. Immunotherapy refers to therapeutics modulating the immune system to elicit an effective immune response. This is a more indirect approach compared to lysing tumors with a chemical. One specific immunotherapy referred to as chimeric antigen receptor (CAR) T-cell therapy is a treatment in which T cells, or cytotoxic immune cells, are engineered to lyse tumor cells. Unfortunately, CAR T-cell therapy is limited due to the tumor’s ability to prevent T cell activation.

Two people born on the same day can age very differently.

Biological age diagnostics help pinpoint the rate a person ages regardless of the amount of time they have spent on earth. This could provide earlier detection of disease for personalised preventative strategies.


Our FREE comprehensive market intelligence report demonstrates how biological age diagnostics are radically transforming how we see and tackle aging.

Equivalent to an 80-year-old human reverting to the age of 26.


A groundbreaking study into anti-aging has reported significant rejuvenation effects using exosomes, tiny particles which can be extracted from biological fluids such as blood plasma.

Old and young rat. Image generated by DALL·E 3

In recent years, the prospect of being able to halt or even reverse aging has begun to seem less like science fiction and more like a scientific milestone that could emerge in the relatively near future.