Scientists found a protein that drives brain aging — and how to stop it
Why it matters: Targeting FTL1 could lead to treatments that reverse age-related memory decline and improve brain function in older individuals.
- FTL1 protein was pinpointed by UC San Francisco researchers as consistently elevated in the hippocampus of older mice, correlating with weakened neural connections and poorer cognitive performance.
- Increased FTL1 levels in young mice mimicked brain aging, causing nerve cells to develop simplified structures instead of complex networks.
- Reducing FTL1 in older mice led to a significant recovery, increasing connections between brain cells and improving memory test performance, described as a "reversal of impairments" by Dr. Saul Villeda.
- FTL1 also impacts cellular metabolism, with higher levels slowing energy use in the hippocampus, a negative effect that was prevented by metabolism-boosting compounds.
Scientists at the University of California - San Francisco have identified a protein, FTL1, as a key driver of brain aging and memory decline in mice, with higher levels weakening neural connections. Remarkably, reducing FTL1 not only reversed these impairments but also restored lost connections and memory function, offering a potential pathway for future brain aging therapies.
