Researchers at the University of California, San Francisco (UCSF) have identified a protein that plays a central role in age-related decline in the hippocampus, the part of the brain responsible for learning and memory.
The team studied changes in genes and proteins within the hippocampus of mice as they aged. They discovered that only one protein, called FTL1, was found at higher levels in older mice compared to younger ones. Older mice with more FTL1 had fewer connections between brain cells and showed decreased cognitive performance.
Experiments revealed that when young mice were engineered to produce more FTL1, their brains and behavior started to resemble those of older animals. In laboratory tests using nerve cells, those with high amounts of FTL1 developed simple neural extensions instead of the usual complex branching patterns.
However, reducing FTL1 levels in the hippocampus of older mice led to significant improvements. The animals formed more connections between nerve cells and performed better on memory assessments.
“It is truly a reversal of impairments,” said Saul Villeda, PhD, associate director of the UCSF Bakar Aging Research Institute and senior author of the paper published in Nature Aging on August 19. “It’s much more than merely delaying or preventing symptoms.”
The research also found that elevated FTL1 slowed down cellular metabolism in the hippocampus. By treating these cells with a compound that boosts metabolism, scientists were able to prevent these negative effects. Villeda expressed hope that these findings could help develop therapies targeting FTL1’s impact on brain aging.
“We’re seeing more opportunities to alleviate the worst consequences of old age,” he said. “It’s a hopeful time to be working on the biology of aging.”
The study was supported by several organizations including the Simons Foundation, Bakar Family Foundation, National Science Foundation, Hillblom Foundation, Bakar Aging Research Institute, Marc and Lynne Benioff, and the National Institutes of Health.
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