Reversing memory loss? The protein scientists hope could turn back the clock on the brain

As the body ages, our physical and mental health deteriorates. Numerous studies have shown that living an active lifestyle, following a healthy diet and doing things to stimulate our cognitive functions all help to slow this decline.

But what if there were basically a switch that you could flip that would reverse aging. It sounds like the stuff of science fiction, but a new study found that by treating the effects of a single protein, it may just be possible. At least for turning back the clock in the brain.

“We’re seeing more opportunities to alleviate the worst consequences of old age. It’s a hopeful time to be working on the biology of aging,” said Saul Villeda, PhD, associate director of the UCSF Bakar Aging Research Institute.

Study opens door to reversing aging in the brain

Researchers at the University of California San Francisco have identified a single protein in brain cells that made the difference in cognitive abilities in mice, regardless of age. Called FTL1, it was found that older mice had more of this protein in their hippocampus, the brain region responsible for learning and memory.

In their study, published in Nature Aging, they showed that increasing the amount of FLT1 in younger mice made their brains function like those of older mice, while at the same time reducing the levels of FTL1 in older mice made them regain their youth.

“It is truly a reversal of impairments. It’s much more than merely delaying or preventing symptoms,” said Villeda, senior author of the paper in press release.

How does FTL1 affect the brain?

The scientists noticed that the older mice, with increased levels of FTL1, besides having diminished cognitive abilities also had fewer connections between brain cells in the hippocampus.

Healthy neurons will grow multiple neurites, or branching wires, that will themselves have several arms that branch out from them. When they performed experiments in petri dishes with nerve cells engineered to produce lots of FTL1 protein, the neurons produced much simpler one-armed neural wires.

The researchers also found that FTL1 slowed metabolism in the cells of the hippocampus of old mice. However, they used a compound to stimulate metabolism to treat the cells which prevented these effects.

This give Villeda hope that their findings could hopefully lead to therapies that can block the adverse effects of FTL1 in the brain.

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