Scientists found a protein that makes the brain age faster: How to arrest its growth

Sunday - 24/08/2025 21:25
A groundbreaking study by UCSF researchers has pinpointed the protein FTL1 as a key contributor to age-related cognitive decline, particularly affecting the hippocampus. Elevated FTL1 levels in older mice correlated with diminished brain cell connections and impaired cognitive function. Remarkably, reducing FTL1 in aged mice reversed these effects, boosting memory and neural connections.
Scientists found a protein that makes the brain age faster: How to arrest its growth
A groundbreaking study by UCSF researchers has pinpointed the protein FTL1 as a key contributor to age-related cognitive decline, particularly affecting the hippocampus. Elevated FTL1 levels in older mice correlated with diminished brain cell connections and impaired cognitive function. Remarkably, reducing FTL1 in aged mice reversed these effects, boosting memory and neural connections.
Aging is often accompanied by a decline in cognitive abilities. These include forgetfulness, difficulty learning, and slower reflexes. So what contributes to an aging brain? A new study has found the culprit behind it. A recent study by researchers at the University of California, San Francisco, has identified a protein that’s at the center of this decline. The findings of the research are published in Nature. Aging and the brain
brain health
The researchers found that a certain protein slows the aging brain, and they know how to counter it. Aging is particularly harsh on the hippocampus, which is the brain region responsible for learning and memory. To understand what aging does to the brain, the researchers looked at the genes and proteins in the hippocampus that changed over time. They observed this in mice model. What they found is significant for further research on aging and cognitive decline. The researchers found that there was one difference between the old and young animals. It was the presence of a protein called FTL1. The researchers observed that the old mice had more FTL1, compared to the younger mice. Interestingly, the presence of FTL1 also led to fewer connections between brain cells in the hippocampus and diminished cognitive abilities.The study
brain
To further understand if FTL1 was the culprit, the researchers artificially elevated FTL1 levels in young mice.
What they found was striking. They noticed that the brains and behavior of the young mice 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 — rather than the branching neurites that normal cells create.When the researchers lowered the levels of FTL1 in the hippocampus of the old mice, surprisingly, they began to regain their youth. The old mice also had more connections between nerve cells, and also responded to memory tests in a better way. “It is truly a reversal of impairments. It’s much more than merely delaying or preventing symptoms,” Saul Villeda, PhD, associate director of the UCSF Bakar Aging Research Institute and senior author of the paper, said, in a statement.
What makes our brain lazy?
They also noticed that the FTL1 slowed down metabolism in the cells of the hippocampus in old mice. But the researchers had found a way to combat it. They treated the cells with a compound that stimulates metabolism and prevented these effects.The researchers are optimistic that their work 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. It’s a hopeful time to be working on the biology of aging,” he said.

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