Scientists Identify Protein That Fuels Brain Ageing

Brain ageing is a complicated process, unlikely to have a single cause. But scientists think they may have found a key piece in the puzzle: protein FTL1.

A study published in Nature Ageing looked at how the brains of mice changed as they aged. They wanted to see what might drive the processes that can slow down our mental activity and impair our memory over the years.

They found that the protein seemed to be the only consistent difference between younger and older mice minds – and they think they know how to counter it.

In older mice, FLT1 levels were higher. They had fewer connections in a part of the brain called the hippocampus (which is responsible for learning and memory), and their cognitive abilities weren’t as high as those of the younger mice.

To investigate whether the protein itself was causing that change, the scientists gave younger mice more of the protein than their bodies naturally made. When they did that, the younger mice had “synaptic changes and cognitive impairments indicative of hippocampal ageing”.

In other words, their brain and behaviours began to mimic those of older mice.

But when they did the inverse – reduced the amount of FLT1 in the brains of older mice – the opposite happened.

They had more connections between nerve cells and performed better on cognitive tests: they seemed, in short, “younger”.

FLT1 slowed metabolism in the hippocampus of older mice. But by giving them a treatment to speed their metabolism up, the scientists were able to prevent that from happening.

They’re hopeful that this might lead to ways to block the effects of the protein in the brain.

In mice, changing FTL1 levels made a bigger difference than just managing the effects of ageing.

Speaking to the University of California, San Francisco, the paper’s senior author, Dr Saul Villeda, said: “It is truly a reversal of impairments. It’s much more than merely delaying or preventing symptoms.”

Though more research is needed to get even close to something like this for humans, Dr Villeda added, “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 ageing.”