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Big news this week: if you played Pokémon as a kid, a study in Nature Human Behaviour says there is a part of your brain that responds specifically to Pokémon. If you go to see Detective Pikachu, you'll have a little bit light up that won't light up in the brains of your parents, or your peers that didn't try to catch them all.

And although that's a pretty cool finding in itself, the discovery also tells researchers a lot about how visual information is stored in our brains. Our ability to easily recognize different objects, whether they're faces or places we've been, is thanks to an area of the brain called the ventral temporal cortex. This area is a kind of filing cabinet where each drawer, or cluster of neurons, contains information about different objects and categories of objects, things like faces or words or places.

Our perception of what we're looking at is based on brain cells in these specific areas firing. And if that firing is messed with, say by applying an electric current directly to the area, our perception gets messed up too. But scientists haven't been sure why certain files show up in certain spots in the brain—why your file for faces is in the same spot as everyone else's, for example.

Many studies have suggested that our brains are trained on objects from an early age— so basically, those files are created when we're kids. But scientists weren't sure whether it was how the objects are viewed or features of the object itself—like how animated or round they are— that decides where in the brain a file for them forms. The leading hypothesis is that what really matters is how the things we see fall on the retina— the part of the eye that transforms light into a pattern of electrical signals for the brain to interpret.

So to test this idea, the authors of this study used people who were die-hard Pokémon fans. You see, pokémon are different enough from other objects, like animals or people, that you'd expect them to have their own file in the ventral temporal cortex. And where that file is, if it exists, could tell scientists whether it's the nature of the object or how we see it that determines location.

So, the team imaged twenty-two adults' brains with an MRI while they looked at pictures of pseudowords, animals, cartoons, hallways, or Pokémon. Half the adults had played lots of Pokémon as a kid and the other half had never played the game. And those that had played the game all had activity in a little fold of the brain called the occipitotemporal sulcus when they looked at pictures of Pokémon characters.

That's really exciting because backs up the retina hypothesis. You see, the scientists assumed people were holding their gaming device at arm's length and focussing on the screen so that the images fell on the center of their visual field on a part of the retina called the fovea. We also do this with faces—we focus on them so they're in the center of our visual field.

And the place in the brain that lit up to Pokémon was really close to the one that lights up for faces, and further from the region that lights up for hallways, which we don't focus on the same way. So not only does seeing objects as a child help build our brains' ability to recognize them, that ability depends on how we're viewing them, too. In addition to validating the current hypothesis, the study also suggests sight in childhood is really important.

The findings could suggest that children who don't or can't focus on objects when they're young, say, because they have cataracts or another eye disorder, may actually code those objects abnormally in their brains, making it harder for them to recognize things later on. In other brain related news, scientists want to reclassify Alzheimer's as a double prion disease, meaning it's caused by two types of incorrectly-folded proteins that infect other proteins and make them misfold too. And this argument has the potential to totally change how neuroscientists diagnose and treat the disease.

Currently, Alzheimer's is thought to be caused by clumps of proteins called beta-amyloid plaques and tangles made of tau proteins. These plaques and tangles seem to disrupt the signalling between brain cells, causing them to lose their function and eventually die, leading to declines in memory and planning that are typical of Alzheimer's. But this new paper, published last week in Science Translational Medicine, argues that modified forms of amyloid and tau act as prions—and that's really what causes all the damage.

According to the paper, amyloid plaques and tau tangles are just the dead remains of these infectious proteins. Now, scientists already had evidence that amyloid plaques could spread from infected brains to healthy ones in the lab, but they thought that was, like, a fluke of the experimental design. They'd also detected prion forms in genetically modified mice with Alzheimer's but dismissed these as a side-effect of having abnormally high levels of disease-causing proteins in general.

This new paper has experimentally shown prion forms of amyloid and tau exist in human brains. But before you freak out, there is no evidence that these prions spread from person to person, just that they spread inside the brain. To come to this conclusion, the researchers in this study took chunks of human brains that had been collected after the people died and ran lab tests on them designed to detect amyloid and tau prion activity.

These tests have only recently been developed, so they haven't been used to examine these prions in human brains before. And they allowed the researchers to compare prion existence and activity in brains affected by Alzheimer's samples to brains from people affected by other dementias and healthy controls. The researchers saw greater amyloid and tau prion activity in Alzheimer's-affected brains, leading the researchers to argue that Alzheimer's is a double prion disorder.

Even more interestingly, people who died younger from a genetic form of the disorder had more prions. For example, the amount of tau prions was correlated with a patient's age at death, while tau tangles were more abundant in older brains in general. One patient, who died at forty, had thirty-two times the concentration of tau prions of someone who died at ninety—which further supports the idea that it's the prions and not the tangles that really cause the disease.

And it may suggest that people with the disease who live longer have special mechanisms that make their brains better at turning harmful prions into plaques or tangles. And that has huge implications for future research, diagnosis, and even potential treatments. In the past, all promising Alzheimer's therapies have failed at the clinical trial stage, and that might be because they had the wrong target.

That is, they were trying to get rid of the dead, leftover proteins rather than the ones actually causing the disease. The authors of this study say we should now be investigating ways to stop these prions from forming or spreading rather than focusing on the tangles and plaques. So, although we've come a long way in our understanding of brains, we're still discovering exactly how these squishy things inside our skulls work—both when we're healthy and when we're not.

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