Aging disrupts memory by increasing levels of the protein FTL1 in the hippocampus, new research shows.
Scientists at UCSF have uncovered a surprising culprit behind brain aging: a protein called FTL1. In mice, too much FTL1 caused memory loss, weaker brain connections, and sluggish cells. But when researchers blocked it, the animals regained youthful brain function and sharp memory. The discovery suggests that one protein could be the master switch for aging in the brain — and targeting it may one day allow us to actually reverse cognitive decline, not just slow it down.
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Take note of the name: ReHMGB1. A new study pinpoints this protein as being able to spread the wear and tear that comes with time as it quietly travels through the bloodstream. This adds significantly to our understanding of aging.
Short for reduced high mobility group box 1, ReHMGB1 triggers senescence in cells, permanently disabling them. It doesn’t just do this locally; it can send damaging signals throughout the body, particularly in response to injuries or disease.
“An important question in aging research is why senescent cells increase with age,” write the study authors, led by researchers from the Korea University College of Medicine.