WEIRDO SCIENCE CORNER: Unfolded issue 03


POkémon grey(matter)

Let’s dig into the nuance here:

The fusiform gyrus is a region in our brain that processes visual information like words, faces, or colors. The thing is, brains are crazy intricate — we don’t fully understand how they store/activate information, and tbh it’s hard to test.

“When a brain is developing, some research has shown that the wiring of our visual cortex is influenced not by the size or shape of something, but rather by its location in our vision and how much of our vision it takes up, a phenomenon known as eccentricity bias.” —via ScienceAlert

>> Think about it: how would you design an experiment to study how human brains store that stuff, especially with all the proper controls? How messed up would it be to force a group of children to stare at precisely the same images for long stretches of time, all at the precisely same brightness + distance from their noses?

Um, so, enter Pokémon Red and Blue for the OG Game Boy, an accidental not-quite-perfect-but-pretty-dang-close experiment (i.e. neuroscientist’s wet dream).

Scientists vetted a group of self-proclaimed Pokémon experts to make sure they knew their Rapidash from their Poliwhirl, then scanned their brain activity (via functional MRI) while showing them images of highways, faces, anipals, words, and Pokémon characters.

In the brains of the gotta-catch-‘em-all connoisseurs, they found a doggone dedicated region for recognizing Pokémon — in their occipitotemporal sulcus. The n00bs’ brains showed no preference for Pokémon.

This study was small, sure, and it may seem like trivial insight (like the discovery of Jennifer Aniston-specific cell clusters in this study). However, the study authors think what they’ve found here might have some implications for understanding aspects of dyslexia, face blindness, or autism.

That’s how science works, anyway: it’ll always beget more questions than answers, and the greatest breakthroughs (imo) materialize through curiosities, accidents, or mistakes.

>> Read more here or here or here, or find the original study here.


A couple of things we know: 1) scientists are curious af. often to a fault. 2) diseases never work the way we expect them to.

Back in the 1700s, yellow fever was a real bummer, killing beaucoup people. In those days, we didn’t really know what viruses and bacteria were, and certainly didn’t have the technology to see them, let alone understand how they work. In fact, the idea of a microscopic organism causing disease was completely absurd.

One of the most prominent theories for diseases at that time was the idea of miasma, “a vaporous exhalation” or “bad air.” Good try, Benjamin Rush, but nah. [Germ theory wasn’t introduced until the mid 1800s.]

After a mega-deadly outbreak of yellow fever in Philadelphia in 1793, our friend Stubbins Ffirth was determined to figure out the cause of yellow fever and how it spreads. [disclaimer: these were the days before regulations / modern-day sense, so, bear with me here.]

Ffirth started by feeding a dog black vomit-soaked bread, who ended up loving the vomit so much he’d eat it bread-free. (so take that?) Ffirth injected animal subjects with black vomit in a variety of ways, which I’ll spare you the details of, and had no luck, so he decided to skip right to testing on himself. I mean, thousands of people had died from this, so it seemed like a great idea to just rub it all over himself, right?

If nothing else, you’ve got to admire his dedication. He introduced black vomit into his body in every way imaginable — pouring “fresh black vomit” into open wounds, dripping it into his eyeballs, breathing in vomit vapor in a DIY vomit sauna, and even having a patient baby bird their vomit right into his mouth! aww.

He eventually concluded that yellow fever was not, in fact, spread by human vomit. It wasn’t until 1901 that U.S. Army surgeon Major Walter Reed proved that the yellow fever virus spreads via the bite of female Aedes Aegypti mosquitoes.

>> Read more here, here, and here.




Cicadas are pretty bonkers. They live below ground as larvae for most of their lives – y’all, we’re talking up to two decades here -- then they zombie crawl their way above ground to live a whopping 2-6 weeks as grownups. They can scream so loud you can hear ‘em up to a mile away. Oh, and if you’re a fangirl, you can track their brooding patterns.

But wait, there’s more. New research from West Virginia University characterized a cicada-infecting fungus that turns cicadas into deranged sex monster zombies.

 ok -> -> Most fungi / fungi-adjacent pathogens are designed to survive, meaning their characteristics have evolved to 1) survive as long as possible and 2) spread to everything it can, thus taking everything it can down with it.

In this case, scientists biochemistry’d the fuck out of Massospra cicadina, this fungus that infects cicadas, to figure out how it works. They identified a plant-associated amphetamine, as well as a chemical not dissimilar from those found in hallucinogenic mushrooms.

It turns out these cicadas first encounter the fungus -- in spore form -- when they’re nestled in their little underground dirt bunkers. Once they’re above ground and the fungus really starts to set in (i.e. full-blown fungal blooms in their bods), that’s when they become [extra] terrifying:

 “The fungus causes cicadas to lose their limbs and eccentric behavior sets in: Males try to mate with everything they encounter, although the fungus has consumed their genitals and butts.” —via WVU Today

Evolution is crazy, though. The fungus encourages infected males to flap their wings in a feminine fashion, “attracting other males to stop by for a quick snuggle.” Snuggle friend is now covered in spores, and the cycle continues, spreading the infection essentially exponentially.

While bizarre and interesting enough on its own, this case is a bit of a head scratcher. It’s super unclear why these mind-altering substances are present at all, especially considering that the usual suspects – the typical genes that encode these things, and the intermediate metabolites that are usually present – aren’t there at all. The next step will be to look at the full genome of the fungus and see how the genes are expressed in healthy vs. infected hosts.

Tbh it’s this stuff, the bizarre oddities and one-offs that have the potential to answer important, yet seemingly unrelated, questions. We’ll see what happens with this one.

>> Read more here, here, here, or here. If you’re so inclined, read the original study here.