Aging is the major risk factor for the development of chronic diseases such as cardiovascular disease, cancer, diabetes, and dementia. Therefore, drugs that slow the aging process may help extend both lifespan and healthspan (the length of time that people are healthy).

In a study published online on February 29 in Medical Research Archives, Albert Einstein College of Medicine researchers evaluated U.S. Food and Drug Administration-approved drugs for their anti-aging potential. In ranking those drugs, they gave equal weight to preclinical studies (i.e., effect on rodent lifespan and healthspan) and clinical studies (i.e., reduced mortality from diseases the drugs were not intended to treat). The four therapeutics judged most promising for targeting aging were SGLT2 inhibitors, metformin, bisphosphonates, and GLP-1 receptor agonists. Since these drugs have been approved for safety and used extensively, the researchers recommend they be evaluated for their anti-aging potential in large-scale clinical trials.

The study’s corresponding author was Nir Barzilai, M.D., director of Einstein’s Institute for Aging Research, professor of medicine and of genetics and the Ingeborg and Ira Leon Rennert Chair in Aging Research at Einstein, and a member of the National Cancer Institute–designated Montefiore Einstein Comprehensive Cancer Center. The lead author was Michael Leone, a medical student at Einstein.

A team led by UT Southwestern Medical Center researchers has discovered a new way that cells regulate senescence, an irreversible end to cell division. The findings, published in Cell, could one day lead to new interventions for a variety of conditions associated with aging, including neurodegenerative and cardiovascular diseases, diabetes, and cancer, as well as new therapies for a collection of diseases known as ribosomopathies.

“There is great interest in reducing senescence to slow or reverse aging or aging-associated diseases. We discovered a noncoding RNA that when inhibited strongly impairs senescence, suggesting that it could be a therapeutic target for conditions associated with aging,” said Joshua Mendell, M.D., Ph.D., Professor of Molecular Biology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. He is also a Howard Hughes Medical Institute Investigator.

Dr. Mendell led the study with co-first authors Yujing Cheng, Ph.D., a recent graduate of the Genetics, Development, and Disease graduate program; and Siwen Wang, M.D., a former postdoctoral researcher, both in the Mendell Lab.

(THE CONVERSATION) Racism steals time from people’s lives – possibly because of the space it occupies in the mind.

Question Is racial discrimination associated with brain connectivity, and are alterations in deep brain functional connectivity associated with accelerated epigenetic aging?

Findings In this cohort study of 90 Black women in the US, higher self-reported racial discrimination was associated with greater resting-state functional connectivity (RSFC) between the locus coeruleus (LC) and precuneus. Significant indirect effects were observed for the association between racial discrimination frequency and DNA methylation age acceleration.

Meaning These findings suggest that racial discrimination is associated with greater connectivity in pathways involved with rumination, which may increase vulnerability to stress-related disorders and neurodegenerative disease via epigenetic age acceleration.