When we’re young, our brains are able to form new neural connections extremely quickly - an ability known as “plasticity” that allows us to learn how to walk, talk and play all in the space of a few years. But, as we get older, this ability fades and, sadly, it takes us longer to learn new things.
Now scientists from Stanford University in the US have managed to unlock child-like plasticity in the adult brains of mice by interfering with a protein known as PirB (or LilrB2 in humans).
The breakthrough is pretty exciting as it could not only lead to new mind-enhancing drugs, but could also help us work out how to make the brain more malleable and better able to recover from damage.
PirB is a receptor that, in both mice and humans, appears to stabilise neural connections. That's useful, as it helps us store information and skills, but it also seems to stop us learning quickly.
In the experiment, a team of scientists led by neurobiologist Carla Shatz interrupted the expression of PirB in the visual cortex of mice’s brains, either through genetic engineering or through a drug known as sPirB - a soluble form of PirB which floods the bloodstream and binds with all of PirB's targets before the protein gets a chance.
These mice, as well as a control group, were then forced to use just one eye - something that requires their brains to rewire in order to recover normal eyesight. In the mice that had PirB activity interrupted, the neural circuits reformed more quickly, and normal eyesight was restored much faster than in the mice whose PirB was functioning normally.
Importantly, the scientists tested the mice both during development and when they were adults - and in each state the mice with interrupted PirB function showed quicker neural rewiring.
The results are published in Science Translational Medicine, and the authors conclude that this is evidence that PirB actively represses neural plasticitiy in the visual cortex of mice - and potentially throughout the brain.
While this is a pretty exciting result, unfortunately things aren't quite so simple in humans - we actually have five different versions of the LilrB2 protein, as Neomatica reports, and scientists will now have to work out which one of those to target in order to unlock similar benefits in our brains.
And, of course, it's yet to be seen what the side effects of blocking the activity of this protein will be in humans.
But it's important research that will help us to understand more about how the brain learns, and also what causes it to slow down. LilrB2 has been linked to Alzheimer's disease in humans, and in the future a similar drug to the one tested in this experiment could potentially help people with the disease.
As for the crazy Limitless-style learning benefits it could unleash in adult humans...we'll have to wait and see.