Well, you're not alone. Chances are, you have misophonia - a condition that can produce strong negative emotions like anger in response to certain trigger noises. Oddly, these triggers almost always involve some sort of facial action like eating, drinking, or even breathing. Fireworks? No problem. Your date slurping their coffee? Feels like the end of the world. This surprising feature of misophonia got some researchers wondering - what if it's not really about the sounds at all? Instead, what if the neural abnormality that causes misophonia actually lies in the part of your brain that controls facial movements?
Interesting. How would you figure that out?
To test this theory, scientists measured the brain activity of “misophonics” in response to trigger noises. It turns out misophonics have fairly typical brain activity in auditory cortex (i.e., the part of your brain that processes sounds), when listening to trigger sounds. However, these trigger noises do seem to cause increased activity in the parts of their brains that control facial muscles. This implies that when misphonics hear someone else chew, they experience a type of hyper-mirroring, or a vicarious experience of the chewing process. The sounds help translate this experience, but the negative reaction is probably not actually about the sounds themselves. Why this leads to such strong negative emotions is still not really understood. But at least now we now know where to focus when designing therapies.
The Leak: We’re one step closer to understanding why the sound of chewing might make your skin crawl. The weird thing is that it may not be about sounds at all, but rather about the facial movements that caused them. If you are interested in learning more about the experiment, you can check out the paper here.
What happened: Earlier this year, the company Neuralink, owned and championed by Elon Musk and his influential tweets, released a video that quickly went viral on twitter and caught the attention of various media sources… and neuroscientists. The video? A monkey playing the game “pong,” by using a brain implant that recorded his neural activity to control the game. Sounds incredible! What a technological feat! Not so fast. Academic labs have been working on this topic for decades. And another company called Blackrock Microsystems, founded by a team of scientists in 2008, has already successfully implemented wireless brain-machine interfaces in human patients with tetraplegia as of this year.
Isn’t this just a couple of geeky companies battling it out for who comes in first?
No. Some are being led to believe that Musk is inventing this and related technologies in neuroscience, which hurts neuroscientists in the long run. Brain-machine interfaces have been under development in academic labs all over the world and evolved from research that goes back to the 1990s. Unfortunately, scientists can’t swing the stock market with their tweets like Musk, so they haven’t had the impact that he has on raising awareness. There’s also been a massive uphill battle to maintain animal research programs that are critical to developing technologies and treatments for human patients. If people don’t understand where the science is actually being done, it won’t get the federal funding resources it needs to continue.
The Leak: Elon funds his pet science projects, he advertises his pet projects…but despite publishing articles by himself (not peer-reviewed by scientists), he doesn’t do science. The technologies he tweets about are products of millions of dollars of research in industry & academia that started decades ago.
No, we’re not talking about some secret spell from Harry Potter. There’s a new FDA approved drug on the block - Aducanumab (seriously, who names these things?) Doctors can now prescribe Aducanumab for Alzheimer’s disease - a devastating illness whose symptoms include memory loss and a decrease in cognitive ability. Usually, a new drug for such a severe illness would be met with cheers and celebration. But this particular approval has raised several objections from neuroscientists.
Why? Don’t they want Alzheimer’s patients to get better?
Well, it's not that simple. Let’s start by taking a quick detour into the biology of Alzheimer’s. A protein known as beta-amyloid can gradually accumulate in the brain over time. In Alzheimer’s patients, the amount of amyloid build-up is unusually excessive. Some researchers have suggested that too much amyloid might hinder the brain’s ability to function, which could lead to the memory loss observed in Alzheimer’s. Evidence supporting this theory is mixed, and additional research is still underway to figure out whether amyloid is indeed the main culprit.
What does this have to do with Aducanumab?
In clinical trials, Aducanumab clearly reduced the amount of amyloid in the brains of people with Alzheimer’s (yay!). Supporters of the drug have pointed to this as the reason for its approval, hoping that reducing amyloid levels could help some patients. However, the clinical trials also failed to clearly show that the drug had an effect on patients’ cognitive ability. Critics believe that this makes the approval premature, especially since reducing the build up of amyloid is meaningless unless it leads to cognitive benefits. One prominent Alzheimer’s researcher even went so far as to call the drug “21st Century Snake Oil” on Twitter.
Sounds confusing. So what happens now?
For what it’s worth, the FDA maintains that there will now be a “phase 4 confirmatory trial” to prove that Aducanumab can improve cognitive function. This trial is likely to take several years so until then, you too can be the proud owner of a an Alzheimer’s drug that maybe-kinda-sorta works for the low price of a mere $60,000 (yikes).
Do you always know whether you’re truly hungry or thirsty? It turns out, we’re pretty bad at eating when hungry and drinking when thirsty, and until recently, scientists weren’t really sure why. A team of researchers have finally uncovered the limitations of how thirst and hunger signals are evaluated, providing scientific evidence for why you might want to actually try that glass of water when you’re unsure.
How did we not know this before?
The short answer is that hunger and thirst are kind of subjective and difficult to study. But this research team decided to try their hand at a little culinary magic and designed an experiment for mice to evaluate their preferences for food and water.
The experiment: Mice were given the option to press a lever to receive either food or water while they were either hungry or thirsty. They ate more food when generally hungry and drank more water while generally thirsty, showing it was possible to measure their food vs. fluid preferences. The researchers then took it up a notch and rapidly alternated the mice between hunger and thirst every few days. This back and forth revealed something interesting: the mice developed a bias for food, regardless of whether they were hungry or thirsty. Based on this, the scientists theorized that the switching could have made it harder for the mice to identify their own physiological needs and led them seek out food by default (similar to how you might reach for a snack when you’re actually thirsty). The researchers then tried to influence the mice’s behavior by manipulating neural activity of a specific brain area - the medial prefrontal cortex (gotta love acronyms, so mPFC). They found that when they suppressed activity in the mPFC, the mice made even poorer decisions, almost as if they were unable to successfully evaluate the outcomes of their choices and relate them back to their needs. For more detail, you can read the paper here or here (free preprint).
The Leak: It turns out, the brain doesn’t always know when you need fuel or fluid, and it determines whether your physiological needs are being met through trial-and-error. So trying a glass of water before going in for seconds might end up being useful after all.
In case you missed it: