- A study found FTL1, an iron-associated protein, plays a role in memory decline in aging mice.
- When researchers lowered the levels of the protein, memory function was restored.
- Researchers believe the protein could be key to treating disorders like Alzheimer's and Parkinson's.
Scientists at the University of California San Francisco say they’ve solved at least part of the mystery surrounding why the brain ages. And they also found a way to stop it.
They say a single protein called FTL1, found in higher levels in aging mice, “weakened connections between the brain cells,” causing memory decline. When the researchers reduced the FTL1 levels, the damage didn’t just stop, but actually began to reverse. “The brain began to recover, rebuilding lost connections and restoring memory performance,” they said in a news release.
FTL1 stands for Ferritin Light Chain 1 protein. It’s an iron-associated protein.
It’s early in the research, as the study was conducted in mice — but mice are often used in studies because of how much they have in common genetically with humans. Still, the findings will at some point need validation in humans if they are to result in treatments.
The study was published in the journal Nature Aging. The researchers said that FTL1 is a “key molecular mediator of cognitive rejuvenation.”
In the study, the researchers looked for changes in genes and proteins in the hippocampus over time, as that part of the brain, which plays a big part in memory and learning, tends to decline in old age. The FTL1 protein, among all they looked at, was the only one that “stood out as consistently different between young and old animals.”
Older mice had more of it. But researchers could also see there were fewer connections between neurons in the hippocampus. And the older mice did not do as well on memory tests.
Per the news release, “When the team boosted FTL1 levels in young mice, the effects were striking. Their brains began to look and function more like those of older mice, and their behavior reflected this shift.”
The reverse was also true. When they lowered the levels of the protein in the older mice, they “showed clear signs of recovery,” including more connections between neurons and better memory test results.
“It is truly a reversal of impairments,” Saul Villeda, associate director of the UC San Francisco Bakar Aging Research Institute and senior author of the paper, said in a written statement. “It’s much more than merely delaying or preventing symptoms.”
They also learned that the protein affects how brain cells use energy, with cellular metabolism slowed in the hippocampus of older mice. The researcher explained that when they added a metabolism-stimulating compound, the aging effects were prevented.
Last August, BBC Science Focus wrote about the UC San Francisco team’s research, noting the possibility it will help target the protein in a way that can be used to treat Parkinson’s and Alzheimer’s disease and other neurodegenerative disorders.
That article said that the protein “plays a role in iron storage and metabolism, keeping long-term levels balanced.” Otherwise the protein begins to build up.
“It’s always interesting when we find something that seems to drive aging, and keeping our brains young is one of the most important aspects of staying healthy and active overall as we get older. FTL1 seems to be such a factor,” anti-ageing expert Andrew Steele told BBC Science Focus.