Genetic research is attempting to explore compounds and develop drugs that could extend the lives of our cells.

We’re living longer these days, but that hasn’t stopped newer branches of medicine from trying to enhance and further extend our lifespans.

Researchers in longevity medicine and biogerontology are studying drugs and compounds that can prevent and reverse aging on the cellular level.

“Over the past few years, public interest in longevity issues has grown, but that interest is mostly in health-extending therapies, not simply life-extending therapies. Most people are interested in living longer, but only if they can also be healthier longer,” Sonia Arrison, author of “100 Plus: How the Coming Age of Longevity Will Change Everything, From Careers and Relationships to Family and Faith,” and founder of Singularity University in California, told Healthline.

While many people are focused on lifestyle changes, the addition of drugs — rapamycin and metformin are two that Arrison mentioned — gives humans more options to extend their lives as well as the quality of their lives.

Compared with preventative drugs such as statins to avoid having a heart attack, anti-aging drugs fight multiple diseases at once instead of focusing on one ailment, Arrison added.

A person who goes by the name Reason, a technologist and author on, which highlights health- and longevity-enhancing medical technologies, told Healthline that the drugs are targeting a wide range of age-related ailments and diseases.

“All age-related diseases are age-related because they are caused by the processes of aging, which is to say an accumulation of damage in cells and tissues,” Reason wrote in an email.

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The field of geroprotection involves understanding cell senescence, which is when cells stop dividing.

When senescent cells no longer divide, they stop functioning, so organ health deteriorates. Cell senescence also causes the release of proinflammatory cytokines, which damage tissues.

This arena involves the use of geroprotectors, which are compounds that can stop or reverse cellular aging, and senolytics, which are compounds that can pinpoint and destroy senescent cells.

This is why researchers are looking into geroprotectors and senolytics, which requires long spans of time to understand.

In essence, today’s researchers may never see the outcomes of the research they’ve started because it can take decades to study. Nevertheless, scientists continue to try to understand these compounds and how they can alter our cells.

Researchers are also looking into our cell’s telomeres, which are short segments of DNA in our chromosomes that protect cells from wear and tear that comes with aging. As cells divide, they can shorten and no longer protect the chromosome or cell.

Lengthening them is the focus of recent research. Last year, a BGRF study was able to lengthen human telomeres.

A recent report in the journal Cell detailed how peptides were able to boost the life span of mice. The study examined how cell therapy could reverse poor age-related kidney function, fur loss, and frailty in mice.

Scientists are looking into whether or not the approach can also prolong the life span of mice. Human safety studies are in the works.

Reason said there are two schools of thought when exploring extending life through genetic pathways.

One approach is to alter cellular metabolism and make cells age more slowly, but the work is difficult and expensive. The other is to fix old tissue because we understand how it compares with young tissue.

“No one yet fully understands everything these [older] cells do to us, but the fastest way to find out is to get rid of them, and we know that doing that in mice extends life and reverts aspects of aging,” Reason explained.

“Either you slow down the damage, or you repair the damage. Aging is damage. It is in the ‘how’ of achieving one of those goals that all the complexity starts up,” Reason added.

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The Human Aging Genomic Resources (HAGR) website recently released DrugAge, a database of lifespan-extending drugs and compounds.

It includes 418 compounds that were recorded from studies on 27 different model organisms.

HAGR already operates the GenAge database of age and longevity-related genes in humans and model organisms. They also operate AnAge, which has aging and longevity records of more than 4,000 species, the GenDR database of genes associated with the life-extending effects of dietary restriction, and LongevityMap, which includes more than 2,000 human gene and genetic variations linked to longevity.

DrugAge incorporates earlier efforts by Biogerontology Research Foundation (BGRF) scientists, who produced Right now, it’s the largest database of its kind.

According to the research teams from BGRF and the University of Liverpool, pharmaceuticals have not targeted most age-related pathways. The research is only focused on a small number of pathways that are currently known.

The goal behind the database is to pave the way for discovery of new life span-extending and health span-extending compounds.

“I am confident that it [DrugAge] will gain widespread use in the aging research community, and represents a significant milestone along the way to the coming paradigm shift in modern healthcare away from single disease treatment and toward geroprotective multi-disease prevention,” Dmitry Kaminskiy, managing trustee of BGRF, said in a statement.

Franco Cortese, deputy director and trustee of BGRF, said in a statement the database will be “extremely valuable” for biogerontologists. The BGRF did not respond to Healthline’s request for comment.

Already, researchers are using the data to identify trends and develop a better understanding of the comparative effects of geroprotectors on organisms.

Arrison is excited when she sees people teaming up globally to battle human disease and decline — something that the DrugAge team is hoping to do with their database.

“The more knowledge the health community can get, the better. The wonderful thing about the internet is that knowledge gets distributed faster, making the quest for cures that much quicker,” Arrison added.

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