Disrupted meiosis, the cell division process that leads to the production of reproductive cells in sexually reproducing organisms, led to a decline in overall health by triggering an accelerating aging signature in the roundworm Caenorhabditis elegans.

The work is “the first direct evidence that manipulating the health of reproductive cells leads to premature aging and a decline in healthspan,” senior author Arjumand Ghazi, an associate professor of pediatrics, developmental biology, and cell biology and physiology at the University of Pittsburgh and the University of Pittsburgh Medical Center (UPMC) Children’s Hospital, said in a press release.

Fibroblasts expressing the tumor suppressor p16INK4a (a marker of senescence) stimulated lung stem cells from young mice to repair damaged tissue, according to a study from the University of California, San Francisco (UCSF). The finding calls into question therapies that eliminate these senescent cells without considering their beneficial role in tissue homeostasis.

By independently manipulating the lifespan of worms and one of its purported biomarkers, namely, the cessation of vigorous movement (CVM), investigators at the Center for Genomic Regulation (CRG) in Barcelona have demonstrated that the two are driven by partly independent processes.

Researchers have gained new insights into both genetic and nongenetic factors affecting life span, and how they differ between males and females. Several genes were correlated with longevity, according to a study by the École Polytechnique Fédérale de Lausanne (EPFL). However, some did not affect life span until males reached a certain age. Early access to nutrients during growth also affected longevity, as they saw in their study of more than 3,000 mice and verified with human data. “This study is one of the biggest studies on mass longevity. We were looking for genetic determinants of longevity but there are non-genetic determinants affecting longevity,” the first author Maroun Bou Sleiman, researcher at EPFL, told Bioworld.

Age-related diseases have been explained as due in part to the excessive generation and accumulation of waste products like the various insoluble protein aggregates observed in nondividing neurons of Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and Huntington’s disease.

Pretzel Therapeutics Inc. has launched with a $72.5 million series A financing to pioneer novel therapies to modulate mitochondrial function to treat rare genetic diseases and common diseases of aging.

A brief pulse of rapamycin before the onset of aging extended lifespan by triggering lasting increases in autophagy. The authors called this phenomenon "rapamycin memory." Elevated autophagy was accompanied by increased levels of LManV and lysozyme in fruit flies, in intestinal enterocytes in female fly models, and its Man2B1 homologue in mice. In mice, a 3-month treatment in early adulthood had the same effect as chronic treatment, even 6 months after rapamycin was withdrawn. In the study published in the Aug. 29, 2022, issue of Nature Aging and led by researchers at the Max Planck Institute, scientists showed that the lifespan-increasing response to rapamycin treatment decreased with the age at which treatment is started.

Scientists have discovered an RNA-based mechanism that is involved in core hallmarks of a number of accelerated aging conditions and shown that therapies targeting this RNA reverses some of these hallmarks in human cells and extend life spans in mouse models.