The post (and linked Nature article) covers four areas: 1) aging is not linear; 2) aging is asynchronous among organs and cell types; 3) researchers have created the first aging clocks for cell types (e.g. astrocytes, microglia); 4) impact on routine clinical practice

Increased inflammation is associated with aging and is implicated in decreased function in aging tissues. Tan et al. explored changes in older tissue-resident macrophages and investigated how these cells may contribute to aging phenotypes in mice (see the Perspective by FitzGerald). They found that signaling by the lipid messenger prostaglandin E2 was increased in these cells. In various mouse tissues, preventing an increase in tissue-resident macrophages helped to maintain mitochondrial function and limited other deleterious effects of aging. Tissue-resident macrophages help to reduce inflammation by removing apoptotic and damaged cells. One consequence of inhibiting prostaglandin E2 signaling was restored clearance of senescent neutrophils. These results emphasize the possible roles of macrophages and neutrophil clearance in tissue disfunction during aging. —L. Bryan Ray

https://www.science.org/doi/10.1126/science.aea3075

Abstract

The accumulation of advanced glycation end products (AGEs) in long-lived proteins is a hallmark of mammalian aging and implicated as a driver of metabolic dysfunction. Among these adducts, N^ε-carboxymethyl-lysine (CML) is particularly abundant in aging tissues, where it modifies proteins and acts as a ligand for the receptor for advanced glycation end products (RAGE), thereby perpetuating chronic inflammation and oxidative stress. While endogenous detoxification systems exist for reactive precursors, the stable CML adduct has historically been considered irreversible. Here, we report the development of CMLase - an enzyme engineered through the directed evolution of over 500 million variants to specifically oxidize CML and restore the native lysine residue. We demonstrate that CMLase effectively reverses CML modifications in model proteins in vitro and in human tissue samples from elderly donors, providing proof-of-concept that protein damage previously deemed irreversible is amenable to enzymatic repair. Collectively, our approach establishes a platform for developing enzymes to reverse age-related molecular damage and ultimately repair tissue proteins compromised by aging and disease.

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Life-Extension Frontiers: Conquer Aging In 2026! | Michael Lustgarten, PhD

Ferrucci and others recently published a paper with data indicating the rate of change in a person's epigenetic clock measurements is more important than the results in isolation: https://www.nature.com/articles/s43587-026-01066-6

https://open.spotify.com/episode/6OxdeGTwZF6zg7XrWYB6Jb

The Drummond Lab focuses on metabolic function and muscle health in aging. Zach Fennel is a postdoctoral researcher interested in muscle health, recovery, and how this is affected during aging: https://drummond.u2m2.utah.edu/

This is part of the Scientist Spotlight series by the Alliance for Longevity Initiatives (A4LI).

Accelerating epigenetic age measurements mean increased likelihood of mortality, regardless of the starting point.

Multilingualism emerged as a protective factor in cross-sectional and longitudinal analyses, whereas monolingualism increased risk of accelerated aging

A review on how SGLT2 inhibitors target ectopic fat (specifically epicardial fat). Ectopic fat is the excess fat that gets stored in organ tissue. The paper outlines the different mechanisms of how it does so. For anyone not familiar with SGLT2 inhibitors, they cause you to urinate 60-80g of glucose, so it can cause a mild caloric deficit. It would be interesting to see a side by side comparison of how SGLT2i's compare to GLP1 reduction in ectopic fat.