Tracking Aging with Practical New Markers [Oct. 21, 2025]

Targeting iron-associated protein Ftl1 in the brain of old mice improves age-related cognitive impairment (Nature Aging, 2025)
Summary: As the brain ages, neuronal ferritin light chain 1　(FTL1) accumulates in the hippocampus, shifting labile iron from Fe²⁺ toward Fe³⁺, lowering metabolic function and ATP production, weakening synaptic activity, and culminating in cognitive decline. Targeting FTL1 improves synaptic and cognitive readouts, supporting FTL1 as a neuronal pro-aging factor that drives cognition loss and as a promising lever for functional rejuvenation.

Highlighted technique: To visualize the redox state of iron in hippocampal tissue, the study used DNAzyme probes in which a fluorophore and a quencher are linked by nucleic acid, and when the DNA reacts at a specific substrate site it is cleaved and the probe lights up. Two probes were applied, one selective for Fe²⁺ and one for Fe³⁺, and the resulting images were combined to map the Fe³⁺/Fe²⁺ ratio and distinguish oxidized and reduced regions in the tissue.

KLRG1 identifies regulatory T cells with mitochondrial alterations that accumulate with aging (Nature Aging, 2025)
Summary: With age, a KLRG1 positive subset of dysfunctional regulatory T cells accumulates in mice and humans, shows mitochondrial abnormalities and DNA damage signals, and exhibits reduced suppressive capacity that links it to age related inflammation. The study positions surface KLRG1 as a practical marker to identify and isolate this population for immune aging readouts and as a potential target to restore inflammatory balance in older individuals.

Highlighted technique: The study shows that KLRG1⁺ regulatory T cells, which accumulate with age, display higher levels of aging markers (p16, p21, γH2AX) and mitochondrial dysfunction, evidenced by reduced membrane potential with fluorescent probes and cristae abnormalities by electron microscopy. In a co-transfer assay into T-cell–deficient mice, these KLRG1⁺ Treg provided weaker protection than KLRG1⁻ Treg, establishing them as a functionally impaired population linked to age-related inflammation.