Finding and testing new longevity medicines, with updates on research, pharma involvement, biomarkers for human trials and the limits of AI.

The peer-reviewed study identified SRSF1 through a transcriptomic screening platform; the lifespan experiment was small, with 9–10 mice per group, so the result is promising but still early.

A string of longevity meetings (ARDD, Biomarkers of Aging, etc.) just wrapped up in Boston and I have to assume some folks here showed up. Please share any highlights!

For decades, reproductive biology and mainstream medicine have treated the ovary almost entirely through the lens of reproduction: periods, pregnancy, and menopause. Once menopause hits, the conventional assumption has been that the organ simply becomes defunct or “retired.”
https://news.northwestern.edu/stories/2026/08-2/reshaping-how-we-think-about-the-ovary-and-aging

The post by Eric Topol explains a recent paper that illuminates biological processes that drive epigenetic drift, which epigenetic clocks can measure across mammals. The original paper lays out the importance of PRC2 in this process (paywalled): https://www.nature.com/articles/s41586-026-10955-0

A Finnish twin study looked at whether living conditions and lifestyle from adolescence to early adulthood were linked to biological aging measured from blood at around age 22.

One interesting finding was that higher youth unemployment in the residential area was linked to faster biological aging. Some measures of nearby vegetation were linked to slower aging, although the environmental results were not always straightforward.

This was an observational study, so it can’t show that these conditions caused faster or slower aging. Biological aging was also measured only once, in early adulthood.

I run a small independent research publication called HUMANUMi, and I wrote more about the study here:

https://humanumi.com/new-study-living-conditions-in-youth-are-linked-to-biological-aging/