Aging can take a toll on memory. Now, a new study has identified a single protein as the culprit of cognitive decline. And scientists believe they may be closer to reversing that decline.
Researchers at the University of California, San Francisco have identified a protein that appears to play a key role in age-related changes in the brain — particularly in the hippocampus, the region responsible for learning and memory.
The protein, known as FTL1, was found at higher levels in older mice, which also showed fewer connections between brain cells and performed worse on cognitive tests.
To better understand its role, scientists increased FTL1 levels in younger mice. Strikingly, their brains began to resemble those of older animals, with reduced neural connections and declines in memory-related behavior.
But the most promising finding came when researchers lowered FTL1 levels in older mice. The animals showed measurable improvement, including stronger connections between neurons and better performance on memory tests.
“It is truly a reversal of impairments,” said senior author Saul Villeda, associate director of the UCSF Bakar Aging Research Institute. “It’s much more than merely delaying or preventing symptoms.”
Further analysis revealed that FTL1 also affects how brain cells use energy. Higher levels of the protein slowed metabolism in the hippocampus, which may contribute to cognitive decline. However, when researchers used a compound to boost cellular metabolism, they were able to counteract these negative effects.
The findings, published in Nature Aging, could open the door to new treatments aimed at preserving — or even restoring — brain function as people age.
“We’re seeing more opportunities to alleviate the worst consequences of old age,” Villeda said. “It’s a hopeful time to be working on the biology of aging.”
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