AI Is Now Designing Aging Therapies That Target Biology Not Just Disease
Immorta Bio is using AI to move beyond disease treatment toward restoring youthful biology by clearing senescent cells and reviving stem cells.
Biological age reversal, epigenetic clocks, senolytics, and anti-aging interventions
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Immorta Bio is using AI to move beyond disease treatment toward restoring youthful biology by clearing senescent cells and reviving stem cells.
A new international conference in Cologne asks whether entropy — the physics of disorder — can unify aging science and point to measurable targets.
An older NIA news story, surfaced again via NIA's longevity topic page, reports that the most optimistic women lived about 4.4 years longer than the least optimistic.
A Nature Aging research highlight points to a systematic review examining the link between physical activity and epigenetic age, though findings are not detailed in the available source.
The creator of epigenetic aging clocks breaks down which interventions—omega-3s, multivitamins, vegetables—reliably shift your biological age.
C. elegans study finds all tested pro-longevity compounds extend male lifespan, but sulforaphane and metformin uniquely preserve late-life reproductive function.
Simple bedside neurological signs present at birth may return in aging and predict dementia up to 7 years before diagnosis.
A new compound stops a damaging protein from crippling brain cell energy factories, slowing Alzheimer's progression and extending lifespan in mice.
Celularity and Fountain Life are offering an investigational cell therapy in Florida under a new state law bypassing FDA approval.
A comprehensive review reveals the thymus retains stem-like epithelial progenitors into adulthood, challenging the idea it is immunologically expendable.
A newly identified extracellular matrix protein accumulates in aging mouse and human brains, triggering microglial inflammation that may accelerate brain decline.
New genome-wide and epidemiological evidence links PM2.5 exposure to shorter telomeres and accelerated aging via causal molecular pathways.