As the brain ages, memory and thinking skills begin to weaken, especially in areas tied to learning and recall. Scientists have long tried to understand what causes these changes, particularly focusing on the hippocampus, a part of the brain that plays a key role in memory. A new study highlights how a protein may contribute to this decline and whether lowering it could help restore brain function.
The research was carried out by scientists at the University of California San Francisco, who tracked age-related changes in the hippocampus of mice over time.
Led by Saul Villeda, PhD, the team focused on identifying differences in hippocampal proteins as mice aged.
Among the many factors they studied, one protein known as FTL1, stood out as consistently higher in older animals, making it a stronger candidate for further study in brain aging.
Mice with higher levels of FTL1 tended to have fewer links between nerve cells in the hippocampus, and they also performed more poorly on memory tests. These findings suggested that FTL1 was not merely accompanying brain aging but could be linked to the loss of connective and cognitive function that often accompanies it.
The researchers found that when nerve cells were pushed to produce large amounts of protein in the lab, their structure became noticeably simpler, with less branching growth seen in healthier cells.
To test that idea more directly, the researchers changed FTL1 levels in living mice.
Increasing the protein levels in younger subjects caused their brains and behavior to age, leading to signs of weaker cognition and a less healthy neural structure. Lowering it in older mice produced the opposite result.
Memory performance improved and connections between brain cells increased, suggesting that reducing FTL1 may help restore functions that had been lost.
“It is truly a reversal of impairments,” Villeda said. “It’s much more than merely delaying or preventing symptoms.”
The study suggests that FTL1 could become an important target in future efforts to address age-related memory decline. The researchers also found signs that the protein may interfere with how cells in the hippocampus handle energy, pointing to a broader role in brain health beyond neural connections alone.
Since the research was done with mice, more research will be needed before the findings can be applied to humans. The results offer a clearer picture of how brain aging may unfold at a molecular level.
“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.”
