EVERWELL

  Scientists at Peking University may have just uncovered a way to tackle one of aging’s most stubborn problems: the build-up of so-called “zombie cells.” These senescent cells, which stop dividing but refuse to die, accumulate in tissues as we grow older. They leak toxic molecules, disrupt healthy cell function, and drive conditions like brittle bones, clogged arteries, fatty liver disease, and even some cancer relapses. Clearing them has long been a dream of the longevity field. Now, a team in Beijing believes they may have found a practical way to do just that  by cutting off the cells’ food supply. What the researchers discovered is that senescent cells share a peculiar weakness. Unlike normal cells, which can make their own supply of the amino acid asparagine, zombie cells lose this ability. They stop producing the enzyme that synthesizes it and instead become entirely dependent on scavenging asparagine from outside sources. It’s as if healthy cells know how to farm thei...

  Aging is often thought of as an inevitable decline, but modern science increasingly shows that it is a carefully regulated process within our cells. Recent research by scientists from the European Research Institute for the Biology of Ageing (ERIBA), using the African turquoise killifish (Nothobranchius furzeri), a species with an exceptionally short lifespan, has shed light on how one gene, CEBPA, can influence both lifespan and healthspan. The findings reveal fundamental principles of cellular regulation that may have relevance far beyond this tiny fish. At the center of this discovery is a protein called C/EBPα, a transcription factor that controls how genes are turned on and off in multiple tissues, including the liver and skin. This protein exists in several forms. One version drives normal cell activity, another acts as a restraint, limiting that activity, and a third, rare form fine-tunes specific cellular functions. The balance between these forms is maintained by a smal...