As people get older, one of the first places in the brain to feel the effects of aging is the hippocampus.
This small but powerful area of the brain is deeply involved in learning and memory, which is why older adults often notice that recalling names, finding the right words, or keeping track of details becomes harder over time.
Scientists have long searched for the reasons behind this decline and whether it can be slowed down or even reversed.
Now, researchers at the University of California, San Francisco (UCSF) have identified a protein that appears to play a central role in the aging of the hippocampus.
In a new study, the team carefully examined how genes and proteins change in the hippocampus as animals grow older. They compared young and old mice and made a surprising discovery: only one protein stood out as being very different. This protein is called FTL1.
In older mice, levels of FTL1 were much higher. At the same time, these mice had fewer connections between brain cells, also called neurons.
With fewer connections, the communication between cells became weaker, which made it harder for the animals to perform memory and learning tasks. Their behavior also showed signs of decline, resembling the kinds of memory problems that humans face in old age.
To understand whether FTL1 was truly responsible for this decline, the scientists tested it in several ways. When they artificially raised FTL1 levels in young mice, those mice began to show brain and behavior changes that looked like aging, even though they were still young.
In lab experiments with nerve cells grown in dishes, cells that produced too much FTL1 grew in strange ways. Instead of creating many branching arms to connect with other cells, they grew only simple, short arms, limiting their ability to form networks.
But the most hopeful part of the research came when the team reduced FTL1 levels in older mice. When FTL1 was lowered, the animals regained more connections between their brain cells. Even more impressive, they performed much better on memory and learning tests, almost as if their brains had turned back the clock.
Dr. Saul Villeda, senior author of the study and associate director of the UCSF Bakar Aging Research Institute, described the findings as more than just slowing aging. He called it a real reversal of age-related impairments.
The team also noticed that FTL1 slowed down the metabolism of cells in the hippocampus, which means the cells were producing less energy and working less efficiently.
When the scientists treated these cells with a compound that boosted metabolism, the negative effects of FTL1 were blocked. This opens the door to possible treatments that either target FTL1 directly or strengthen cell metabolism to protect the brain.
Although this research was done in mice, it gives new hope for understanding human brain aging. If scientists can find safe ways to reduce or block FTL1 in people, it might one day be possible to prevent or even reverse some of the memory loss linked to aging.
Dr. Villeda expressed optimism, saying that discoveries like this are opening more opportunities to fight the toughest challenges of old age.
The findings highlight just how powerful a single protein can be in shaping brain health. While aging is a natural process, this study suggests that at least some of its effects on memory may be treatable. Future research will be needed to see if the results in mice can be repeated in humans, but for now, it marks an exciting step forward in the science of aging.
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