For many, getting older can unfortunately mean an increased risk of illness from cardiovascular disease to cancer. University of Michigan scientists are actively researching the biological underpinnings of aging with the aim of developing interventions that could potentially help people live longer, healthier lives.

A new paper in the journal Science Advances describes the discovery of several promising small molecules that appear to reduce cellular stress in mouse skin cells and could lengthen life.

“Cellular stress resistance appears to be a common feature of long-lived organisms, such as invertebrates and mice,” says the paper’s lead author David Lombard, M.D., Ph.D., associate professor of pathology. Lombard is part of a multidisciplinary group at U-M’s Paul F. Glenn Center for Aging. Recent research from colleague and fellow study author Richard Miller, M.D., Ph.D., found several promising drugs, including rapamycin, a cancer drug, and acarbose, a diabetes drug, that extended life in mice.

Every human being is home to trillions of microbes that are collectively known as the microbiota. Recent research into how these microbes affect the immune system may explain why older people are more vulnerable to disease and suggest ways to tackle that vulnerability.

Scientists at The University of Edinburgh’s Roslin Institute, led by Professor Neil Mabbott, discovered that as mice get older they showed a marked decrease in the number of M cells found in the lining of the gut. These are specialised cells that look out for infections and trigger the early stages of the immune response. Fewer M cells means a weaker immune system. At the same time, the researchers found that the older mice had depleted microbiota compared to younger mice. The microbiota were less diverse and certain species known to decrease inflammation of the gut in humans were missing.

In a study of gorilla skeletons collected in the wild, Johns Hopkins Medicine researchers and their international collaborators report that aging female gorillas do not experience the accelerated bone loss associated with the bone-weakening condition called osteoporosis, as their human counterparts often do. The findings, they say, could offer clues as to how humans evolved with age-related diseases.

The study was published on Sept. 21, 2020, in Philosophical Translations of the Royal Society B.

“Osteoporosis in humans is a really interesting mechanical problem,” says Christopher Ruff, Ph.D., professor at the Center for Functional Anatomy and Evolution at the Johns Hopkins University School of Medicine. “In terms of natural selection, there is no evolutionary advantage in developing bone loss with aging to the point of a potential fracture. By looking at close relatives of humans on the evolutionary tree, we can infer more about the origins of this condition.”