Each week, we read what's going on the world of science and bring the wildest findings straight to you. This week, just for fun, we’re focusing on animals. Animal studies don’t always translate successfully to human health, but they’re still incredibly important. Humans are complicated, and understanding how the mind and body work in other creatures can help pave the way for treatments in people.
A microbe helped mouse models of autism restore their social behaviors
One of the features of autism spectrum disorder (ASD) is that a person will have difficulties in social interactions and behavior. In a new study published in Neuron, researchers found that giving a bacteria, L. reuteri, to mice bred to have similar symptoms as ASD was able to reverse these social interaction problems. It’s another piece of evidence that what goes on in our guts has a powerful influence on our minds.
ASD almost surely has several causes: genetic, environmental, or idiopathic— idiopathic meaning that the cause is unknown or comes out of nowhere. There are mouse models to represent each of these causes, and the researchers wanted to see if their bacteria could improve social behaviors in each one, says Mauro Costa-Mattioli, the director of the Memory and Brain Research Center at Baylor College of Medicine and author on the paper.
When they gave L. reuteri to each of the three mouse ASD models, it restored social behaviors in all of them, “suggesting that this microbial-based approach could improve social behavior in a wider subset of ASD,” a release says.
When they looked closer to see how the L. reuteri was affecting social behavior, they found that the microbes interacted with the brain through the vagus nerve, which connects the gut and the brain. When the researchers cut this nerve, L. reuteri no longer changed social behavior.
They also found that the bacteria are most likely making this difference by producing oxytocin, a hormone associated with social interactions, because when they genetically engineered mice to be missing oxytocin receptors, it also prevented the effects of the L. reuteri.
These are experiments that couldn’t be done in humans—you wouldn’t ethically be able to cut a person’s vagus nerve, or genetically delete their oxytocin receptors. So studying the mechanisms of L. reuteri in mouse models helps us understand what the bacteria are really doing to the brain before we try anything in people.
They are currently discussing with a clinician the possibility of introducing the bacteria in humans, but “this needs to be done very carefully,” Costa-Mattioli tells me. “We think that our findings have strengthened the rather unconventional idea that it might be possible to modulate specific behavior through the gut microbiome using select bacterial strains,” he says in the release.
Deleting a gene in mice lets them eat as much fat as they want, and not get fat themselves
We’d all love to eat as much as we want and never gain weight, and in mice with a certain gene removed, that dream came true. In a paper published in EMBO Reports, a gene called RCAN1 was removed in mice. After, when they were fed a high fat diet, they didn’t gain any weight—even after stuffing their face with fat for long periods of time.
The authors aren’t just trying to give us no-consequence cheat days. “We were trying to answer the question about which of our genes are responsible for people getting fat, so that we might identify new ways to tackle the obesity problem,” says Damien Keating, a principal research fellow and the Centre for Neuroscience at Flinders University in Australia.
When mice were placed on high fat diets and did become obese, Keating and his colleagues noticed that the gene expression of RCAN1 was the most increased in important metabolic places like the liver and fat cells. When they silenced the RCAN1 gene, they found that mice didn’t gain any weight—not because they ate less or were more active, “but because they burn more calories at rest,” Keating tells me.
RCAN1 causes fat cells to store more fat and burn less energy. It also works in skeletal muscle, which is responsible for around 30 percent of our resting energy use, to reduce the amount of energy consumed by muscle. In the mice where RCAN1 wasn’t doing its job, the opposite was occurring.
“The overall picture seems to be that when we (mice only have been studied here) eat a high calorie diet, RCAN1 expression increases in places like fat cells, and this causes us to burn less calories at rest and to store more fat,” Keating says.
Humans do have the same RCAN1 gene, and Keating thinks that because of this, their findings are relevant to human health. They’re currently testing drugs that target these pathways and processes in humans to help people lose weight and help alleviate health conditions like diabetes, heart disease, stroke, cancer, and high blood pressure associated with obesity.
There are clues in tortoise DNA as to why they live so long
On a Sunday morning in June 2012, a tortoise named Lonesome George was found dead stretched out in the direction of his watering hole. Lonesome George was the only known Pinta Island tortoise left in the world, and lived at a conservation center in the Galapagos Islands. When he died, his species died with him. He was around 100 years old.
But "Lonesome George is still teaching us lessons," Adalgisa Caccone, a senior researcher in Yale's Department of Ecology and Evolutionary Biology, said in a press release. In a new study, Caccone and her colleagues used Lonesome George’s DNA to look for clues to how he—and other tortoises—can live so long. Giant tortoises often live to be more than 100 years old, while other vertebrates have life spans a fraction of that.
The research, published in Nature Ecology & Evolution , compared Lonesome George’s DNA with other DNA samples from giant tortoises of the Galapagos and found that the tortoises have several gene variants linked with longevity.
There are several genetic features that lead to longer lifespan, and nine have been described, says Victor Fernandez, first author of the paper and a postdoctoral researcher at University of Oviedo in Spain. These include things like having DNA repair genes, inflammatory mediators, and genes related to cancer development, the paper says.
“We chose 500 human genes which were known to be related to these hallmarks and looked for their tortoise counterparts,” Fernandez tells me. “In about a dozen tortoise genes, we found changes in the sequence as compared to humans that might change the way they act. Those changes are predicted to affect six of those nine hallmarks, including cell proliferation and DNA damage repair. This suggests future experiments that may give us information on how these hallmarks regulate aging.”
Since the scientists looked for genetic variants that were first identified in humans, it could mean that learning how they work in another species might help in translating what they found to people. The study hints at evolutionary strategies for longer lifespan, and could help us get a better grasp at what makes an animal live for 100 years, or for 20.
“I think a comparative approach as the one used in this study can provide useful insights, as we are looking at what likely are very evolutionary conserved process,” Caccone says. “ After all the human and tortoise lineages split more than 300 millions of years ago. So if we find some variants in human and tortoises associated with longevity and age-related diseases, this may be a clue that tells us that these variants are involved in this trait and it is worth pursuing in further detail.”
Giving monkeys ketamine treats one of the worst symptoms of depression
One of the most debilitating symptoms of depression is anhedonia, which is the loss of pleasure. People don't feel excited about things they used to love. But the way the brain changes during anhedonia isn’t well known. Without knowing what’s gone wrong, it’s hard to fix.
In a new study in marmoset monkeys, an overactive region in the brain has been associated with anhedonia, and when those monkeys were given ketamine, it was shown that the drug acted on that same area—offering a hint as to why ketamine might be such an effective antidepressant.
The research, published in Neuron, found that over-activity in an area of the monkey’s frontal lobes dulls the excitement of an anticipated reward, and also the motivation to work for that reward, a press release says. Marmoset monkeys are often used to study brain disorders because they have similar frontal lobes to humans.
The monkeys were trained to respond to sounds, one sound would give them a treat (a marshmallow), and the other wouldn’t. Once they learned that one sound meant they got a marshmallow, they would become excited when they heard it, but wouldn’t show the same level of excitement for the second sound.
The monkeys were then given a drug to make parts of their frontal lobes active, or they were given a placebo. The monkeys that got the drug showed less excitement and anticipation at getting a marshmallow, even though they still ate it. When the monkeys had to push a button repeatedly to get their marshmallow, the monkeys given the drug gave up sooner than those without. When the researchers looked at their brains, they saw that the overactivity caused by drug had an effect in other brain regions, possibly leading to the diminished anticipation.
Finally, the monkeys were given ketamine 24 hours before doing the experiment again. This time, even the monkeys that got the drugs were excited about their marshmallows. The brain imaging showed that “the brain circuits were functioning normally,” a release says. “In other words, ketamine had blocked the effects of over-activating area…which would otherwise blunt anticipation.”
"By revealing the specific symptoms and brain circuits that are sensitive to antidepressants like ketamine, this study moves us one step closer to understanding how and why patients may benefit from different treatments,” says Laith Alexander, the study's first author in the release.
Your weekly health and reading list
The placenta, an afterthought no longer. By Apoorva Mandavilli in The New York Times
It has been called “afterbirth,” and then thrown away– but recent studies on the placenta show there’s a lot more to learn about this “ephemeral organ.”
Five diets that could be deadly. By Sara Chodosh and Claire Maldarelli in Popular Science.
We love to fixate on extreme diets for health, but doing so—whether it’s keto, paleo, or Whole30—can end up hurting us more than helping.
Welcome to the trip of your life: the rise of underground LSD guides. By Carey Dunne in The Guardian.
How can you find a professional to guide you for your LSD trip, when LSD is illegal?
What humpback whales can teach us about alien languages. By Brian Resnick in Vox.
“Scientists don’t know what, exactly, these whales and dolphins are saying to one another. But they suspect what they are vocalizing is, perhaps, a language, because it mimics a mathematical pattern shared by all languages on Earth.”
Living apart, coming undone. By Joaquin Sapien, ProPublica, and Tom Jennings for Frontline in ProPublica.
A sad, important story of what happened when hundreds of severely mentally ill people were moved out of institutions into private apartments in New York City.
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