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Aging is especially harsh on the hippocampus — the brain regionโข responsible for learning and โฃmemory. Now, researchers at โUC san Francisco have identified a protein that’s at the center of this decline. They looked at how the genesโ and proteinsโค in the hippocampus changed over time in mice and found just one thatโข differed between old and young animals. It’s called FTL1. Old mice hadโ more FTL1, as well as fewer โconnections between brain cells in the hippocampus and diminished cognitive abilities. When the researchers โขartificially increased FTL1 levels in young mice,โ their brains and behavior began to resemble that of old mice. In experiments in petri dishes, nerve cells engineered to make lots of FTL1 grew simple, one-armed neurites — ratherโฃ than the branching neurites that normal cellsโ create. But once โtheโ scientists reduced the amountโค of FTL1 โคin the hippocampus of โคthe old mice, theyโฃ regained their youth. They had moreโ connections between nerve cells, and the mice did better on memory tests. “It is trulyโ a reversal of impairments,” said Saul Villeda, PhD,โ associate director of the UCSF bakar Aging Research Instituteโ and senior author of theโค paper, wich appears in โข Nature Aging on august 19. “It’s much more than merely delaying or preventing symptoms.” In old โฃmice, FTL1 โฃalso slowed down metabolism in โthe cells โขof theโ hippocampus. But treatingโ the cells with a compoundโ that stimulates metabolism prevented these effects. Villeda is optimistic the workโ could lead to therapies that block the effects of FTL1 in the brain. “We’re seeing more opportunities to alleviate the worst consequences of old age,” he said. “It’s a hopeful โtime to be working on the biology of aging.” Authors: Other UCSF authors are Laura Remesal, PhD, Juliana Sucharov-Costa, Karishma โคJ.B. Pratt,PhD,Gregor Bieri,PhD,Amber Philp,PhD,Mason Phan,turan Aghayev,MD,PhD,Charles W. White III, PhD, Elizabeth G. Wheatley, PhD, Brandon R. Desousa,Isha H. Jian, Jason C. Maynard, phd, and Alma L. burlingame,โ phd. Funding: This work was funded in part by the Simons Foundation,โ bakar family Foundation, National Science Foundation, Hillblom Foundation, Bakar Aging Research Institute, Marc and Lynne Benioff, andโ the National Institutes of Health (AG061038,โ AG067740, AG062357,โฃ P30 DK063720).