Many MindedBoosting one brain-cell protein appears to slow aging across mouse bodies
A study in Aging Cell reports that raising fibroblast growth factor 13 (FGF13) in astrocytes slows aging across the whole body in mice. Lifespan.io covered it in an article by Josh Conway dated October 29, 2026.
FGF13 is a non-secreted member of the FGF family and works independently of the FGF receptor. Public mouse datasets showed it falls with age in oligodendrocytes, astrocytes and microglia, but not neurons. In the hippocampus it declined steadily; in the cortex it rose at 6 months before declining. Macaque data were less complete but similar, with an especially strong drop in astrocytes. Knocking out FGF13 in astrocytes of aging mice worsened water maze performance, increased senescence in heart, skin, liver, spleen and kidney, and raised circulating inflammatory cytokines. Raising it in old mice brought water maze performance close to that of young mice, improved elevated plus maze and open field results (not to young levels), lowered blood IFN-γ and IL-6, reduced senescence in skin, liver, spleen and kidney (not heart), and reduced age-related weight gain.
The proposed mechanism runs through astrocyte health. FGF13-deficient astrocytes had higher complement C3 and Cx43, impaired neuronal synapses in co-culture, and prompted microglia to release inflammatory factors; overexpression reversed this. FGF13 binds Phafin2, an autophagy-related protein that also declines with age in mice, and raising FGF13 raised Phafin2 and autophagy markers P62 and LC3.
For health, this points to the brain as a possible lever on body-wide aging, a target that might someday help delay age-related disease. That is a long way off. The evidence is from mice and cell culture, with macaque data limited to observing FGF13 levels, not testing treatment. The paper offers no way to raise FGF13 in human astrocytes, and most peripheral benefits were significant but modest. Watch for replication and any delivery approach.
Source: Lifespan.io