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Martha Carlin married the love of her life in 1995. She and John Carlin had dated briefly in college in Kentucky, then lost touch until a chance meeting years later at a Dallas pub. They wed soon after and had two children. John worked as an entrepreneur and stay-at-home dad. In his free time, he ran marathons.

Almost eight years into their marriage, the pinky finger on John’s right hand began to quiver. So did his tongue. Most disturbing for Martha was how he looked at her. For as long as she’d known him, he’d had a joy in his eyes. But then, she says, he had a stony stare, “like he was looking through me.” In November 2002, a doctor diagnosed John with Parkinson’s disease. He was 44 years old.

Carlin made it her mission to understand how her seemingly fit husband had developed such a debilitating disease. “The minute we got home from the neurologist, I was on the internet looking for answers,” she recalls. She began consuming all of the medical literature she could find.

With her training in accounting and corporate consulting, Carlin was used to thinking about how the many parts of large companies came together as a whole. That kind of wide-angle perspective made her skeptical that Parkinson’s, which affects half a million people in the United States, was just a malfunction in the brain.Martha Carlin married the love of her life in 1995. She and John Carlin had dated briefly in college in Kentucky, then lost touch until a chance meeting years later at a Dallas pub. They wed soon after and had two children. John worked as an entrepreneur and stay-at-home dad. In his free time, he ran marathons.

Almost eight years into their marriage, the pinky finger on John’s right hand began to quiver. So did his tongue. Most disturbing for Martha was how he looked at her. For as long as she’d known him, he’d had a joy in his eyes. But then, she says, he had a stony stare, “like he was looking through me.” In November 2002, a doctor diagnosed John with Parkinson’s disease. He was 44 years old.

Carlin made it her mission to understand how her seemingly fit husband had developed such a debilitating disease. “The minute we got home from the neurologist, I was on the internet looking for answers,” she recalls. She began consuming all of the medical literature she could find.

With her training in accounting and corporate consulting, Carlin was used to thinking about how the many parts of large companies came together as a whole. That kind of wide-angle perspective made her skeptical that Parkinson’s, which affects half a million people in the United States, was just a malfunction in the brain.
“I had an initial hunch that food and food quality was part of the issue,” she says. If something in the environment triggered Parkinson’s, as some theories suggest, it made sense to her that the disease would involve the digestive system. Every time we eat and drink, our insides encounter the outside world.

John’s disease progressed slowly and Carlin kept up her research. In 2015, she found a paper titled, “Gut microbiota are related to Parkinson’s disease and clinical phenotype.” The study, by neurologist Filip Scheperjans of the University of Helsinki, asked two simple questions: Are the microorganisms that populate the guts of Parkinson’s patients different than those of healthy people? And if so, does that difference correlate with the stooped posture and difficulty walking that people with the disorder experience? Scheperjans’ answer to both questions was yes.

Carlin had picked up on a thread from one of the newest areas of Parkinson’s research: the relationship between Parkinson’s and the gut. Other than a small fraction of cases that are inherited, the cause of Parkinson’s disease is unknown. What is known is that something kills certain nerve cells, or neurons, in the brain. Abnormally misfolded and clumped proteins are the prime suspect. Some theories suggest a possible role for head trauma or exposure to heavy metals, pesticides or air pollution.
People with Parkinson’s often have digestive issues, such as constipation, long before the disease appears. Since the early 2000s, scientists have been gathering evidence that the malformed proteins in the brains of Parkinson’s patients might actually first appear in the gut or nose (people with Parkinson’s also commonly lose their sense of smell).
From there, the theory goes, these proteins work their way into the nervous system. Scientists don’t know exactly where in the gut the misfolded proteins come from, or why they form, but some early evidence points to the body’s internal microbial ecosystem. In the latest salvo, scientists from Sweden reported in October that people who had their appendix removed had a lower risk of Parkinson’s years later (SN: 11/24/18, p. 7). The job of the appendix, which is attached to the colon, is a bit of a mystery. But the organ may play an important role in intestinal health.

If the gut connection theory proves true — still a big if — it could open up new avenues to one day treat or at least slow the disease.

“It really changes the concept of what we consider Parkinson’s,” Scheperjans says. Maybe Parkinson’s isn’t a brain disease that affects the gut. Perhaps, for many people, it’s a gut disease that affects the brain.

Gut feeling
London physician James Parkinson wrote “An essay on the shaking palsy” in 1817, describing six patients with unexplained tremors. Some also had digestive problems. (“Action of the bowels had been very much retarded,” he reported of one man.) He treated two people with calomel — a toxic, mercury-based laxative of the time — and noted that their tremors subsided.

But the digestive idiosyncrasies of the disease that later bore Parkinson’s name largely faded into the background for the next two centuries, until neuroanatomists Heiko Braak and Kelly Del Tredici, now at the University of Ulm in Germany, proposed that Parkinson’s disease might arise from the intestine. Writing in Neurobiology of Aging in 2003, they and their colleagues based their theory on autopsies of Parkinson’s patients.
The researchers were looking for Lewy bodies, which contain clumps of a protein called alpha-synuclein. The presence of Lewy bodies in the brain is a hallmark of Parkinson’s, though their exact role in the disease is still under investigation.

Lewy bodies form when alpha-synuclein, which is produced by neurons and other cells, starts curdling into unusual strands. The body encapsulates the abnormal alpha-synuclein and other proteins into the round Lewy body bundles. In the brain, Lewy bodies collect in the cells of the substantia nigra, a structure that helps orchestrate movement. By the time symptoms appear, much of the substantia nigra is already damaged.

Substantia nigra cells produce the chemical dopamine, which is important for movement. Levodopa, the main drug prescribed for Parkinson’s, is a synthetic replacement for dopamine. The drug has been around for a half-century, and while it can alleviate symptoms for a while, it does not slow the destruction of brain cells.

In patient autopsies, Braak and his team tested for the presence of Lewy bodies, as well as abnormal alpha-s­ynuclein that had not yet become bundled together. Based on comparisons with people without Parkinson’s, the researchers found signs that Lewy bodies start to form in the nasal passages and intestine before they show up in the brain. Braak’s group proposed that Parkinson’s disease develops in stages, migrating from the gut and nose into the nerves to reach the brain.

Neural highway
Today, the idea that Parkinson’s might arise from the intestine, not the brain, “is one of the most exciting things in Parkinson’s disease,” says Heinz Reichmann, a neurologist at the University of Dresden in Germany. The Braak theory couldn’t explain how the Lewy bodies reach the brain, but Braak speculated that some sort of pathogen, perhaps a virus, might travel along the body’s nervous system, leaving a trail of Lewy bodies.

There is no shortage of passageways: The intestine contains so many nerves that it’s sometimes called the body’s second brain. And the vagus nerve offers a direct connection between those nerves in the gut and the brain (SN: 11/28/15, p. 18).

In mice, alpha-synuclein can indeed migrate from the intestine to the brain, using the vagus nerve like a kind of intercontinental highway, as Caltech researchers demonstrated in 2016 (SN: 12/10/16, p. 12). And Reichmann’s experiments have shown that mice that eat the pesticide rotenone develop symptoms of Parkinson’s. Other teams have shown similar reactions in mice that inhale the chemical. “What you sniff, you swallow,” he says.

To look at this idea another way, researchers have examined what happens to Parkinson’s risk when people have a weak or missing vagus nerve connection. There was a time when doctors thought that an overly eager vagus nerve had something to do with stomach ulcers. Starting around the 1970s, many patients had the nerve clipped as an experimental means of treatment, a procedure called a vagotomy. In one of the latest studies on vagotomy and Parkinson’s, researchers examined more than 9,000 patients with vagotomies, using data from a nationwide patient registry in Sweden. Among people who had the nerve cut down low, just above the stomach, the risk of Parkinson’s began dropping five years after surgery, eventually reaching a difference of about 50 percent compared with people who hadn’t had a vagotomy, the researchers reported in 2017 in Neurology.
The studies are suggestive, but by no means definitive. And the vagus nerve may not be the only possible link the gut and brain share. The body’s immune system might also connect the two, as one study published in January in Science Translational Medicine found. Study leader Inga Peter, a genetic epidemiologist at the Icahn School of Medicine at Mount Sinai in New York City, was looking for genetic contributors to Crohn’s disease, an inflammatory bowel condition that affects close to 1 million people in the United States.

She and a worldwide team studied about 2,000 people from an Ashkenazi Jewish population, which has an elevated risk of Crohn’s, and compared them with people without the disease. The research led Peter and colleagues to suspect the role of a gene called LRRK2. That gene is involved in the immune system — which mistakenly attacks the intestine in people who have Crohn’s. So it made sense for a variant of that gene to be involved in inflammatory disease. The researchers were thrown, however, when they discovered that versions of the gene also appeared to increase the risk for Parkinson’s disease.

“We refused to believe it,” Peter says. The finding, although just a correlation, suggested that whatever the gene was doing to the intestine might have something to do with Parkinson’s. So the team investigated the link further, reporting results in the August JAMA Neurology.

In their analysis of a large database of health insurance claims and prescriptions, the scientists found more evidence of inflammation’s role. People with inflammatory bowel disease were about 30 percent more likely to develop Parkinson’s than people without it. But among those who had filled prescriptions for an anti-inflammatory medication called antitumor necrosis factor, which the researchers used as a marker for reduced inflammation, Parkinson’s risk was 78 percent lower than in people who had not filled prescriptions for the drug.

Belly bacteria
Like Inga Peter, microbiologist Sarkis Mazmanian of Caltech came upon Parkinson’s disease almost by accident. He had long studied how the body’s internal bacteria interact with the immune system. At lunch one day with a colleague who was studying autism using a mouse version of the disease, Mazmanian asked if he could take a look at the animals’ intestines. Because of the high density of nerves in the intestine, he wanted to see if the brain and gut were connected in autism.

Neurons in the gut “are literally one cell layer away from the microbes,” he says. “That made me feel that at least the physical path or conduit was there.” He began to study autism, but wanted to switch to a brain disease with more obvious physical symptoms. When he learned that people with Parkinson’s disease often have a long history of digestive problems, he had his subject.

Mazmanian’s group examined mice that were genetically engineered to overproduce alpha-synuclein. He wanted to know whether the presence or absence of gut bacteria influenced symptoms that developed in the mice.

The results, reported in Cell in 2016, showed that when the mice were raised germ free — meaning their insides had no microorganisms — they showed no signs of Parkinson’s. The animals had no telltale gait or balance problems and no constipation, even though their bodies made alpha-synuclein (SN: 12/24/16 & 1/7/17, p. 10). “All the features of Parkinson’s in the animals were gone when the animals had no microbiome,” he says.

However, when gut microbes from people diagnosed with Parkinson’s were transplanted into the germ-free mice, the mice developed symptoms of the disease — symptoms that were much more severe than those in mice transplanted with microbes from healthy people.

Mazmanian suspects that something in the microbiome triggers the misfolding of alpha-synuclein. But this has not been tested in humans, and he is quick to say that this is just one possible explanation for the disease. “There’s likely no one smoking gun,” he says.

Microbial forces
If the microbiome is involved, what exactly is it doing to promote Parkinson’s? Microbiologist Matthew Chapman of the University of Michigan in Ann Arbor thinks it may have something to do with chemical signals that bacteria send to the body. Chapman studies biofilms, which occur when bacteria form resilient colonies. (Think of the slime on the inside a drain pipe.)

Part of what makes biofilms so hard to break apart is that fibers called amyloids run through them. Amyloids are tight stacks of proteins, like columns of Legos. Scientists have long suspected that amyloids are involved in degenerative diseases of the brain, including Alzheimer’s. In Parkinson’s, amyloid forms of alpha-synuclein are found in Lewy bodies.

Despite amyloids’ bad reputation, the fibers themselves aren’t always undesirable, Chapman says. Sometimes they may provide a good way of storing proteins for future use, to be snapped off brick by brick as needed. Perhaps it’s only when amyloids form in the wrong place, like the brain, that they contribute to disease. Chapman’s lab group has found that E. coli bacteria, part of the body’s normal microbial population, produce amyloid forms of some proteins when they are under stress.

When gut bacteria produce amyloids, the body’s own cells could also be affected, wrote Chapman in 2017 in PLOS Pathogens with an unlikely partner: neurologist Robert Friedland of the University of Louisville School of Medicine in Kentucky. “This is a difficult field to study because it’s on the border of several fields,” Friedland says. “I’m a neurologist who has little experience in gastro­enterology. When I talked about this to my colleagues who are gastroenterologists, they’ve never heard that bacteria make amyloid.”
Friedland and collaborators reported in 2016 in Scientific Reports that when E. coli in the intestines of rats started to produce amyloid, alpha-synuclein in the rats’ brains also congealed into the amyloid form. In their 2017 paper, Chapman and Friedland suggested that the immune system’s reaction to the amyloid in the gut might have something to do with triggering amyloid formation in the brain.

In other words, when gut bacteria get stressed and start to produce their own amyloids, those microbes may be sending cues to nearby neurons in the intestine to follow suit. “The question is, and it’s still an outstanding question, what is it that these bacteria are producing that is, at least in animals, causing alpha-synuclein to form amyloids?” Chapman says.

Head for a cure
There is, in fact, a long list of questions about the microbiome, says Scheperjans, the neurologist whose paper Martha Carlin first spotted. So far, studies of the microbiomes of human patients are largely limited to simple observations like his, and the potential for a microbiome connection has yet to reach deeply into the neurology community. But in O­ctober, for the second year in a row, Scheperjans says, the International Congress of Parkinson’s Disease and Movement Disorders held a panel discussing connections to the microbiome.

“I got interested in the gastrointestinal aspects because the patients complained so much about it,” he says. While his study found definite differences in the bacteria of people with Parkinson’s, it’s still too early to know how that might matter. But Scheperjans hopes that one day doctors may be able to test for microbiome changes that put people at higher risk for Parkinson’s, and restore a healthy microbe population through diet or some other means to delay or prevent the disease.
One way to slow the disease might be shutting down the mobility of misfolded alpha-synuclein before it has even reached the brain. In Science in 2016, neuroscientist Valina Dawson and colleagues at Johns Hopkins University School of Medicine and elsewhere described using an antibody to halt the spread of bad alpha-synuclein from cell to cell. The researchers are working now to develop a drug that could do the same thing.

The goal is to one day test for the early development of Parkinson’s and then be able to tell a patient, “Take this drug and we’re going to try to slow and prevent progression of disease,” she says.

For her part, Carlin is doing what she can to speed research into connections between the microbiome and Parkinson’s. She quit her job, sold her house and drained her retirement account to pour money into the cause. She donated to the University of Chicago to study her husband’s microbiome. And she founded a company called the BioCollective to aid in microbiome research, providing free collection kits to people with Parkinson’s. The 15,000 microbiome samples she has collected so far are available to researchers.

Carlin admits that the possibility of a gut connection to Parkinson’s can be a hard sell. “It’s a difficult concept for people to wrap their head around when you are taking a broad view,” she says. As she searches for answers, her husband, John, keeps going. “He drives, he runs biking programs in Denver for people with Parkinson’s,” she says. Anything to keep the wheels turning toward the future.One way to slow the disease might be shutting down the mobility of misfolded alpha-synuclein before it has even reached the brain. In Science in 2016, neuroscientist Valina Dawson and colleagues at Johns Hopkins University School of Medicine and elsewhere described using an antibody to halt the spread of bad alpha-synuclein from cell to cell. The researchers are working now to develop a drug that could do the same thing.

The goal is to one day test for the early development of Parkinson’s and then be able to tell a patient, “Take this drug and we’re going to try to slow and prevent progression of disease,” she says.

For her part, Carlin is doing what she can to speed research into connections between the microbiome and Parkinson’s. She quit her job, sold her house and drained her retirement account to pour money into the cause. She donated to the University of Chicago to study her husband’s microbiome. And she founded a company called the BioCollective to aid in microbiome research, providing free collection kits to people with Parkinson’s. The 15,000 microbiome samples she has collected so far are available to researchers.

Carlin admits that the possibility of a gut connection to Parkinson’s can be a hard sell. “It’s a difficult concept for people to wrap their head around when you are taking a broad view,” she says. As she searches for answers, her husband, John, keeps going. “He drives, he runs biking programs in Denver for people with Parkinson’s,” she says. Anything to keep the wheels turning toward the future.

Race should no longer be used to describe populations in most genetics studies, a panel of experts says.

Using race and ethnicity to describe study participants gives the mistaken impression that humans can be divided into distinct groups. Such labels have been used to stigmatize groups of people, but do not explain biological and genetic diversity, the panel convened by the U.S. National Academies of Sciences, Engineering and Medicine said in a report on March 14.
In particular, the term Caucasian should no longer be used, the committee recommends. The term, coined in the 18th century by German scientist Johann Friedrich Blumenbach to describe what he determined was the most beautiful skull in his collection, carries the false notion of white superiority, the panel says.

Worse, the moniker “has also acquired today the connotation of being an objective scientific term, and that’s what really led the committee to take objection with it,” says Ann Morning, a sociologist at New York University and a member of the committee that wrote the report. “It tends to reinforce this erroneous belief that racial categories are somehow objective and natural characterizations of human biological difference. We felt that it was a term that … should go into the dustbin of history.”

Similarly, the term “black race” shouldn’t be used because it implies that Black people are a distinct group, or race, that can be objectively defined, the panel says.

Racial definitions are problematic “because not only are they stigmatizing, they are historically wrong,” says Ambroise Wonkam, a medical geneticist at Johns Hopkins University and president of the African Society of Human Genetics. Race is often used as a proxy for genetic diversity. But “race cannot be used to capture diversity at all. Race doesn’t exist. There is only one race, the human race,” says Wonkam, who was not involved with the National Academies’ panel.

Race might be used in some studies to determine how genetic and social factors contribute to health disparities (SN: 4/5/22), but beyond that race has no real value in genetic research, Wonkam adds.

Researchers could use other identifiers, including geographical ancestry, to define groups of people in the study, Wonkam says. But those definitions need to be precise.

For instance, some researchers group Africans by language groups. But a Bantu-speaking person from Tanzania or Nigeria where malaria is endemic would have a much higher genetic risk of sickle cell disease than a Bantu-speaking person whose ancestors are from South Africa, where malaria has not existed for at least 1,000 years. (Changes in genes that make hemoglobin can protect against malaria (SN: 5/2/11), but cause life-threatening sickle cell disease.)
Genetic studies also have to account for movements of people and mixture between multiple groups, Wonkam says. And labeling must be consistent for all groups in the study, he says. Current studies sometimes compare continent-wide racial groups, such as Asian, with national groups, such as French or Finnish, and ethnic groups, such as Hispanic.

An argument for keeping race in rare cases
Removing race as a descriptor may be helpful for some groups, such as people of African descent, says Joseph Yracheta, a health disparities researcher and the executive director of the Native BioData Consortium, headquartered on the Cheyenne River Sioux reservation in South Dakota. “I understand why they want to get rid of race science for themselves, because in their case it’s been used to deny them services,” he says.

But Native Americans’ story is different, says Yracheta, who was not part of the panel. Native Americans’ unique evolutionary history have made them a valuable resource for genetics research. A small starting population and many thousands of years of isolation from humans outside the Americas have given Native Americans and Indigenous people in Polynesia and Australia some genetic features that may make it easier for researchers to find variants that contribute to health or disease, he says. “We’re the Rosetta stone for the rest of the planet.”

Native Americans “need to be protected, because not only are our numbers small, but we keep having things taken away from us since 1492. We don’t want this to be another casualty of colonialism.” Removing the label of Indigenous or Native American may erode tribal sovereignty and control over genetic data, he says.

The panel does recommend that genetic researchers should clearly state why they used a particular descriptor and should involve study populations in making decisions about which labels to use.

That community input is essential, Yracheta says. The recommendations have no legal or regulatory weight. So he worries that this lack of teeth may allow researchers to ignore the wishes of study participants without fear of penalty.

Still seeking diversity in research participants
Genetics research has suffered from a lack of diversity of participants (SN: 3/4/21). To counteract the disparities, U.S. government regulations require researchers funded by the National Institutes of Health to collect data on the race and ethnicity of study participants. But because those racial categories are too broad and don’t consider the social and environmental conditions that may affect health, the labels are not helpful in most genetic analyses, the panel concluded.

Removing racial labels won’t hamper diversity efforts, as researchers will still seek out people from different backgrounds to participate in studies, says Brendan Lee, who is president of the American Society of Human Genetics. But taking race out of the equation should encourage researchers to think more carefully about the type of data they are collecting and how it might be used to support or refute racism, says Lee, a medical geneticist at Baylor College of Medicine in Houston, who was not part of the panel.

The report offers decision-making tools for determining what descriptors are appropriate for particular types of studies. But “while it is a framework, it is not a recipe where in every study we do A, B and C,” Lee says.

Researchers probably won’t instantly adopt the new practices, Lee says. “It is a process that will take time. I don’t think it is something we can expect in one week or one evening that we’ll all change over to this, but it is a very important first step.”

Just a few powerful storms in Antarctica can have an outsized effect on how much snow parts of the southernmost continent get. Those ephemeral storms, preserved in ice cores, might give a skewed view of how quickly the continent’s ice sheet has grown or shrunk over time.

Relatively rare extreme precipitation events are responsible for more than 40 percent of the total annual snowfall across most of the continent — and in some places, as much as 60 percent, researchers report March 22 in Geophysical Research Letters.
Climatologist John Turner of the British Antarctic Survey in Cambridge and his colleagues used regional climate simulations to estimate daily precipitation across the continent from 1979 to 2016. Then, the team zoomed in on 10 locations — representing different climates from the dry interior desert to the often snowy coasts and the open ocean — to determine regional differences in snowfall.

While snowfall amounts vary greatly by location, extreme events packed the biggest wallop along Antarctica’s coasts, especially on the floating ice shelves, the researchers found. For instance, the Amery ice shelf in East Antarctica gets roughly half of its annual precipitation — which typically totals about half a meter of snow — in just 10 days, on average. In 1994, the ice shelf got 44 percent of its entire annual precipitation on a single day in September.

Ice cores aren’t just a window into the past; they are also used to predict the continent’s future in a warming world. So characterizing these coastal regions is crucial for understanding Antarctica’s ice sheet — and its potential future contribution to sea level rise.
Editor’s note: This story was updated April 5, 2019, to correct that the results were reported March 22 (not March 25).

We live in a sea of neutrinos. Every second, trillions of them pass through our bodies. They come from the sun, nuclear reactors, collisions of cosmic rays hitting Earth’s atmosphere, even the Big Bang. Among fundamental particles, only photons are more numerous. Yet because neutrinos barely interact with matter, they are notoriously difficult to detect.

The existence of the neutrino was first proposed in the 1930s and then verified in the 1950s (SN: 2/13/54). Decades later, much about the neutrino — named in part because it has no electric charge — remains a mystery, including how many varieties of neutrinos exist, how much mass they have, where that mass comes from and whether they have any magnetic properties.
These mysteries are at the heart of Ghost Particle by physicist Alan Chodos and science journalist James Riordon. The book is an informative, easy-to-follow introduction to the perplexing particle. Chodos and Riordon guide readers through how the neutrino was discovered, what we know — and don’t know — about it, and the ongoing and future experiments that (fingers crossed) will provide the answers.

It’s not just neutrino physicists who await those answers. Neutrinos, Riordon says, “are incredibly important both for understanding the universe and our existence in it.” Unmasking the neutrino could be key to unlocking the nature of dark matter, for instance. Or it could clear up the universe’s matter conundrum: The Big Bang should have produced equal amounts of matter and antimatter, the oppositely charged counterparts of electrons, protons and so on. When matter and antimatter come into contact, they annihilate each other. So in theory, the universe today should be empty — yet it’s not (SN: 9/22/22). It’s filled with matter and, for some reason, very little antimatter.

Science News spoke with Riordon, a frequent contributor to the magazine, about these puzzles and how neutrinos could act as a tool to observe the cosmos or even see into our own planet. The following conversation has been edited for length and clarity.

SN: In the first chapter, you list eight unanswered questions about neutrinos. Which is the most pressing to answer?

Riordon: Whether they’re their own antiparticles is probably one of the grandest. The proposal that neutrinos are their own antiparticles is an elegant solution to all sorts of problems, including the existence of this residue of matter we live in. Another one is figuring out how neutrinos fit in the standard model [of particle physics]. It’s one of the most successful theories there is, but it can’t explain the fact that neutrinos have mass.
SN: Why is now a good time to write a book about neutrinos?

Riordon: All of these questions about neutrinos are sort of coming to a head right now — the hints that neutrinos may be their own antiparticles, the issues of neutrinos not quite fitting the standard model, whether there are sterile neutrinos [a hypothetical neutrino that is a candidate for dark matter]. In the next few years, a decade or so, there will be a lot of experiments that will [help answer these questions,] and the resolution either way will be exciting.

SN: Neutrinos could also be used to help scientists observe a range of phenomena. What are some of the most interesting questions neutrinos could help with?

Riordon: There are some observations that simply have to be done with neutrinos, that there are no other technological alternatives for. There’s a problem with using light-based telescopes to look back in history. We have this really amazing James Webb Space Telescope that can see really far back in history. But at some point, when you go far enough back, the universe is basically opaque to light; you can’t see into it. Once we narrow down how to detect and how to measure the cosmic neutrino background [neutrinos that formed less than a second after the Big Bang], it will be a way to look back at the very beginning. Other than with gravitational waves, you can’t see back that far with anything else. So it’ll give us sort of a telescope back to the beginning of the universe.

The other thing is, when a supernova happens, all kinds of really cool stuff happens inside, and you can see it with neutrinos because neutrinos come out immediately in a burst. We call it the “cosmic neutrino bomb,” but you can track the supernova as it’s going along. With light, it takes a while for it to get out [of the stellar explosion]. We’re due for a [nearby] supernova. We haven’t had one since 1987. It was the last visible supernova in the sky and was a boon for research. Now that we have neutrino detectors around the world, this next one is going to be even better [for research], even more exciting.

And if we develop better instrumentation, we could use neutrinos to understand what’s going on in the center of the Earth. There’s no other way that you could probe the center of the Earth. We use seismic waves, but the resolution is really low. So we could resolve a lot of questions about what the planet is made of with neutrinos.

SN: Do you have a favorite “character” in the story of neutrinos?

Riordon: I’m certainly very fond of my grandfather Clyde Cowan [he and Frederick Reines were the first physicists to detect neutrinos]. But Reines is a riveting character. He was poetic. He was a singer. He really was this creative force. I mentioned [in the book] that they put this “SNEWS” sign on their detector for “supernova early warning system,” which sort of echoed the ballistic missile early warning systems at the time [during the Cold War]. That’s so ripe.

For the first time, astronomers have caught a glimpse of shock waves rippling along strands of the cosmic web — the enormous tangle of galaxies, gas and dark matter that fills the observable universe.

Combining hundreds of thousands of radio telescope images revealed the faint glow cast as shock waves send charged particles flying through the magnetic fields that run along the cosmic web. Spotting these shock waves could give astronomers a better look at these large-scale magnetic fields, whose properties and origins are largely mysterious, researchers report in the Feb. 17 Science Advances.
Finally, astronomers “can confirm what so far has only been predicted by simulations — that these shock waves exist,” says astrophysicist Marcus Brüggen of the University of Hamburg in Germany, who was not involved in the new study.

At its grandest scale, our universe looks something like Swiss cheese. Galaxies aren’t distributed evenly through space but rather are clumped together in enormous clusters connected by ropy filaments of dilute gas, galaxies and dark matter and separated by not-quite-empty voids (SN: 10/3/19).

Tugged by gravity, galaxy clusters merge, filaments collide, and gas from the voids falls onto filaments and clusters. In simulations of the cosmic web, all that action consistently sets off enormous shock waves in and along filaments.

Filaments make up most of the cosmic web but are much harder to spot than galaxies (SN: 1/20/14). While scientists have observed shock waves around galaxy clusters before, shocks in filaments “have never been really seen,” says astronomer Reinout van Weeren of Leiden University in the Netherlands, who was not involved in the study. “But they should be basically all around the cosmic web.”

Shock waves around filaments would accelerate charged particles through the magnetic fields that suffuse the cosmic web (SN: 6/6/19). When that happens, the particles emit light at wavelengths that radio telescopes can detect — though the signals are very weak.
A single shock wave in a filament “would look like nothing, it’d look like noise,” says radio astronomer Tessa Vernstrom of the International Centre for Radio Astronomy Research in Crawley, Australia.

Instead of looking for individual shock waves, Vernstrom and her colleagues combined radio images of more than 600,000 pairs of galaxy clusters close enough to be connected by filaments to create a single “stacked” image. This amplified weak signals and revealed that, on average, there is a faint radio glow from the filaments between clusters.

“When you can dig below the noise and still actually get a result — to me, that’s personally exciting,” Vernstrom says.

The faint signal is highly polarized, meaning that the radio waves are mostly aligned with one another. Highly polarized light is unusual in the cosmos, but it is expected from radio light cast by shock waves, van Weeren says. “So that’s really, I think, very good evidence for the fact that the shocks are likely indeed present.”
The discovery goes beyond confirming the predictions of cosmic web simulations. The polarized radio emissions also offer a rare peek at the magnetic fields that permeate the cosmic web, if only indirectly.

“These shocks,” Brüggen says, “are really able to show that there are large-scale magnetic fields that form [something] like a sheath around these filaments.”

He, van Weeren and Vernstrom all note that it’s still an open question how cosmic magnetic fields arose in the first place. The role these fields play in shaping the cosmic web is equally mysterious.

“It’s one of the four fundamental forces of nature, right? Magnetism,” Vernstrom says. “But at least on these large scales, we don’t really know how important it is.”

For generations of dogs, home is the radioactive remains of the Chernobyl Nuclear Power Plant.

In the first genetic analysis of these animals, scientists have discovered that dogs living in the power plant industrial area are genetically distinct from dogs living farther away.

Though the team could distinguish between dog populations, the researchers did not pinpoint radiation as the reason for any genetic differences. But future studies that build on the findings, reported March 3 in Science Advances, may help uncover how radioactive environments leave their mark on animal genomes.
That could have implications for other nuclear disasters and even human space travel, says Timothy Mousseau, an evolutionary ecologist at the University of South Carolina in Columbia. “We have high hopes that what we learn from these dogs … will be of use for understanding human exposures in the future,” he says.

Since his first trip in 1999, Mousseau has stopped counting how many times he’s been to Chernobyl. “I lost track after we hit about 50 visits.”

He first encountered Chernobyl’s semi-feral dogs in 2017, on a trip with the Clean Futures Fund+, an organization that provides veterinary care to the animals. Not much is known about how local dogs survived after the nuclear accident. In 1986, an explosion at one of the power plant’s reactors kicked off a disaster that lofted vast amounts of radioactive isotopes into the air. Contamination from the plant’s radioactive cloud largely settled nearby, in a region now called the Chernobyl Exclusion Zone.

Dogs have lived in the area since the disaster, fed by Chernobyl cleanup workers and tourists. Some 250 strays were living in and around the power plant, among spent fuel-processing facilities and in the shadow of the ruined reactor. Hundreds more roam farther out in the exclusion zone, an area about the size of Yosemite National Park.
During Mousseau’s visits, his team collected blood samples from these dogs for DNA analysis, which let the researchers map out the dogs’ complex family structures. “We know who’s related to who,” says Elaine Ostrander, a geneticist at the National Human Genome Research Institute in Bethesda, Md. “We know their heritage.”

The canine packs are not just a hodgepodge of wild feral dogs, she says. “There are actually families of dogs breeding, living, existing in the power plant,” she says. “Who would have imagined?”

Dogs within the exclusion zone share ancestry with German shepherds and other shepherd breeds, like many other free-breeding dogs from Eastern Europe, the team reports. And though their work revealed that dogs in the power plant area look genetically different from dogs in Chernobyl City, about 15 kilometers away, the team does not know whether radiation caused these differences or not, Ostrander says. The dogs may be genetically distinct simply because they’re living in a relatively isolated area.

The new finding is not so surprising, says Jim Smith, an environmental scientist at the University of Portsmouth in England. He was not part of the new study but has worked in this field for decades. He’s concerned that people might assume “that the radiation has something to do with it,” he says. But “there’s no evidence of that.”

Scientists have been trying to pin down how radiation exposure at Chernobyl has affected wildlife for decades (SN: 5/2/14). “We’ve been looking at the consequences for birds and rodents and bacteria and plants,” Mousseau says. His team has found animals with elevated mutation rates, shortened life spans and early-onset cataracts.

It’s not easy to tease out the effects of low-dose radiation among other factors, Smith says. “[These studies] are so hard … there’s lots of other stuff going in the natural environment.” What’s more, animals can reap some benefits when humans leave contaminated zones, he says.

How, or if, radiation damage is piling up in dogs’ genomes is something the team is looking into now, Ostrander says. Knowing the dogs’ genetic backgrounds will make it easier to spot any radiation red flags, says Bridgett vonHoldt, an evolutionary geneticist at Princeton University, who was not involved in the work.

“I feel like it’s a cliffhanger,” she says. “I want to know more.”

To shrink error rates in quantum computers, sometimes more is better. More qubits, that is.

The quantum bits, or qubits, that make up a quantum computer are prone to mistakes that could render a calculation useless if not corrected. To reduce that error rate, scientists aim to build a computer that can correct its own errors. Such a machine would combine the powers of multiple fallible qubits into one improved qubit, called a “logical qubit,” that can be used to make calculations (SN: 6/22/20).

Scientists now have demonstrated a key milestone in quantum error correction. Scaling up the number of qubits in a logical qubit can make it less error-prone, researchers at Google report February 22 in Nature.
Future quantum computers could solve problems impossible for even the most powerful traditional computers (SN: 6/29/17). To build those mighty quantum machines, researchers agree that they’ll need to use error correction to dramatically shrink error rates. While scientists have previously demonstrated that they can detect and correct simple errors in small-scale quantum computers, error correction is still in its early stages (SN: 10/4/21).

The new advance doesn’t mean researchers are ready to build a fully error-corrected quantum computer, “however, it does demonstrate that it is indeed possible, that error correction fundamentally works,” physicist Julian Kelly of Google Quantum AI said in a news briefing February 21.
Logical qubits store information redundantly in multiple physical qubits. That redundancy allows a quantum computer to check if any mistakes have cropped up and fix them on the fly. Ideally, the larger the logical qubit, the smaller the error rate should be. But if the original qubits are too faulty, adding in more of them will cause more problems than it solves.

Using Google’s Sycamore quantum chip, the researchers studied two different sizes of logical qubits, one consisting of 17 qubits and the other of 49 qubits. After making steady improvements to the performance of the original physical qubits that make up the device, the researchers tallied up the errors that still slipped through. The larger logical qubit had a lower error rate, about 2.9 percent per round of error correction, compared to the smaller logical qubit’s rate of about 3.0 percent, the researchers found.
That small improvement suggests scientists are finally tiptoeing into the regime where error correction can begin to squelch errors by scaling up. “It’s a major goal to achieve,” says physicist Andreas Wallraff of ETH Zurich, who was not involved with the research.

However, the result is only on the cusp of showing that error correction improves as scientists scale up. A computer simulation of the quantum computer’s performance suggests that, if the logical qubit’s size were increased even more, its error rate would actually get worse. Additional improvement to the original faulty qubits will be needed to enable scientists to really capitalize on the benefits of error correction.

Still, milestones in quantum computation are so difficult to achieve that they’re treated like pole jumping, Wallraff says. You just aim to barely clear the bar.

Inspired by how ants move through narrow spaces by shortening their legs, scientists have built a robot that draws in its limbs to navigate constricted passages.

The robot was able to hunch down and walk quickly through passages that were narrower and shorter than itself, researchers report January 20 in Advanced Intelligent Systems. It could also climb over steps and move on grass, loose rock, mulch and crushed granite.

Such generality and adaptability are the main challenges of legged robot locomotion, says robotics engineer Feifei Qian, who was not involved in the study. Some robots have specialized limbs to move over a particular terrain, but they cannot squeeze into small spaces (SN: 1/16/19).
“A design that can adapt to a variety of environments with varying scales or stiffness is a lot more challenging, as trade-offs between the different environments need to be considered,” says Qian, of the University of Southern California in Los Angeles.

For inspiration, researchers in the new study turned to ants. “Insects are really a neat inspiration for designing robot systems that have minimal actuation but can perform a multitude of locomotion behaviors,” says Nick Gravish, a roboticist at the University of California, San Diego (SN: 8/16/18). Ants adapt their posture to crawl through tiny spaces. And they aren’t perturbed by uneven terrain or small obstacles. For example, their legs collapse a bit when they hit an object, Gravish says, and the ants continue to move forward quickly.

Gravish and colleagues built a short, stocky robot — about 30 centimeters wide and 20 centimeters long — with four wavy, telescoping limbs. Each limb consists of six nested concentric tubes that can draw into each other. What’s more, the limbs do not need to be actively powered or adjusted to change their overall length. Instead, springs that connect the leg segments automatically allow the legs to contract when the robot navigates a narrow space and stretch back out in an open space. The goal was to build mechanically intelligent structures rather than algorithmically intelligent robots.

“It’s likely faster than active control, [which] requires the robot to first sense the contact with the environment, compute the suitable action and then send the command to its motors,” Qian says, about these legs. Removing the sensing and computing components can also make the robots small, cheap and less power hungry.

The robot could modify its body width and height to achieve a larger range of body sizes than other similar robots. The leg segments contracted into themselves to let the robot wiggle through small tunnels and sprawled out when under low ceilings. This adaptability let the robot squeeze into spaces as small as 72 percent its full width and 68 percent its full height.
Next, the researchers plan to actively control the stiffness of the springs that connect the leg segments to tune the motion to terrain type without consuming too much power. “That way, you can keep your leg long when you are moving on open ground or over tall objects, but then collapse down to the smallest possible shape in confined spaces,” Gravish says.
Such small-scale, minimal robots are easy to produce and can be quickly tweaked to explore complex environments. However, despite being able to walk across different terrains, these robots are, for now, too fragile for search-and-rescue, exploration or biological monitoring, Gravish says.

The new robot takes a step closer to those goals, but getting there will take more than just robotics, Qian says. “To actually achieve these applications would require an integration of design, control, sensing, planning and hardware advancement.”

But that’s not Gravish’s interest. Instead, he wants to connect these experiments back to what was observed in the ants originally and use the robots to ask more questions about the rules of locomotion in nature (SN: 1/16/20).

“I really would like to understand how small insects are able to move so rapidly across certain unpredictable terrain,” he says. “What is special about their limbs that enables them to move so quickly?”

The dwarf planet Quaoar has a ring that is too big for its metaphorical fingers. While all other rings in the solar system lie within or near a mathematically determined distance of their parent bodies, Quaoar’s ring is much farther out.

“For Quaoar, for the ring to be outside this limit is very, very strange,” says astronomer Bruno Morgado of the Federal University of Rio de Janeiro. The finding may force a rethink of the rules governing planetary rings, Morgado and colleagues say in a study published February 8 in Nature.
Quaoar is an icy body about half the size of Pluto that’s located in the Kuiper Belt at the solar system’s edge (SN: 8/23/22). At such a great distance from Earth, it’s hard to get a clear picture of the world.

So Morgado and colleagues watched Quaoar block the light from a distant star, a phenomenon called a stellar occultation. The timing of the star winking in and out of view can reveal details about Quaoar, like its size and whether it has an atmosphere.

The researchers took data from occultations from 2018 to 2020, observed from all over the world, including Namibia, Australia and Grenada, as well as space. There was no sign that Quaoar had an atmosphere. But surprisingly, there was a ring. The finding makes Quaoar just the third dwarf planet or asteroid in the solar system known to have a ring, after the asteroid Chariklo and the dwarf planet Haumea (SN: 3/26/14; SN: 10/11/17).

Even more surprisingly, “the ring is not where we expect,” Morgado says.
Known rings around other objects lie within or near what’s called the Roche limit, an invisible line where the gravitational force of the main body peters out. Inside the limit, that force can rip a moon to shreds, turning it into a ring. Outside, the gravity between smaller particles is stronger than that from the main body, and rings will coalesce into one or several moons.

“We always think of [the Roche limit] as straightforward,” Morgado says. “One side is a moon forming, the other side is a ring stable. And now this limit is not a limit.”

For Quaoar’s far-out ring, there are a few possible explanations, Morgado says. Maybe the observers caught the ring at just the right moment, right before it turns into a moon. But that lucky timing seems unlikely, he notes.

Maybe Quaoar’s known moon, Weywot, or some other unseen moon contributes gravity that holds the ring stable somehow. Or maybe the ring’s particles are colliding in such a way that they avoid sticking together and clumping into moons.

The particles would have to be particularly bouncy for that to work, “like a ring of those bouncy balls from toy stores,” says planetary scientist David Jewitt of UCLA, who was not involved in the new work.

The observation is solid, says Jewitt, who helped discover the first objects in the Kuiper Belt in the 1990s. But there’s no way to know yet which of the explanations is correct, if any, in part because there are no theoretical predictions for such far-out rings to compare with Quaoar’s situation.

That’s par for the course when it comes to the Kuiper Belt. “Everything in the Kuiper Belt, basically, has been discovered, not predicted,” Jewitt says. “It’s the opposite of the classical model of science where people predict things and then confirm or reject them. People discover stuff by surprise, and everyone scrambles to explain it.”

More observations of Quaoar, or more discoveries of seemingly misplaced rings elsewhere in the solar system, could help reveal what’s going on.

“I have no doubt that in the near future a lot of people will start working with Quaoar to try to get this answer,” Morgado says.

Today’s red jungle fowl — the wild forebears of the domesticated chicken — are becoming more chickenlike. New research suggests that a large proportion of the wild fowl’s DNA has been inherited from chickens, and relatively recently.

Ongoing interbreeding between the two birds may threaten wild jungle fowl populations’ future, and even hobble humans’ ability to breed better chickens, researchers report January 19 in PLOS Genetics.

Red jungle fowl (Gallus gallus) are forest birds native to Southeast Asia and parts of South Asia. Thousands of years ago, humans domesticated the fowl, possibly in the region’s rice fields (SN: 6/6/22).
“Chickens are arguably the most important domestic animal on Earth,” says Frank Rheindt, an evolutionary biologist at the National University of Singapore. He points to their global ubiquity and abundance. Chicken is also one of the cheapest sources of animal protein that humans have.

Domesticated chickens (G. gallus domesticus) were known to be interbreeding with jungle fowl near human settlements in Southeast Asia. Given the unknown impacts on jungle fowl and the importance of chickens to humankind, Rheindt and his team wanted to gather more details. Wild jungle fowl contain a store of genetic diversity that could serve as a crucial resource for breeding chickens resistant to diseases or other threats.

The researchers analyzed and compared the genomes — the full complement of an organism’s DNA — of 63 jungle fowl and 51 chickens from across Southeast Asia. Some of the jungle fowl samples came from museum specimens collected from 1874 through 1939, letting the team see how the genetic makeup of jungle fowl has changed over time.

Over the last century or so, wild jungle fowl’s genomes have become increasingly similar to chickens’. Between about 20 and 50 percent of the genomes of modern jungle fowl originated in chickens, the team found. In contrast, many of the roughly 100-year-old jungle fowl had a chicken-ancestry share in the range of a few percent.

The rapid change probably comes from human communities expanding into the region’s wilderness, Rheindt says. Most modern jungle fowl live in close vicinity to humans’ free-ranging chickens, with which they frequently interbreed.

Such interbreeding has become “almost the norm now” for any globally domesticated species, Rheindt says, such as dogs hybridizing with wolves and house cats crossing with wildcats. Pigs, meanwhile, are mixing with wild boars and ferrets with polecats.
Wild populations that interbreed with their domesticated counterparts could pick up physical or behavioral traits that change how the hybrids function in their ecosystem, says Claudio Quilodrán, a conservation geneticist at the University of Geneva not involved with this research.

The effect is likely to be negative, Quilodrán says, since some of the traits coming into the wild population have been honed for human uses, not for survival in the local environment.

Wild jungle fowl have lost their genetic diversity as they’ve interbred too. The birds’ heterozygosity — a measure of a population’s genetic diversity — is now just a tenth of what it was a century ago.

“This result is initially counterintuitive,” Rheindt says. “If you mix one population with another, you would generally expect a higher genetic diversity.”

But domesticated chickens have such low genetic diversity that certain versions of jungle fowl genes are being swept out of the population by a tsunami of genetic homogeneity. The whittling down of these animals’ genetic toolkit may leave them vulnerable to conservation threats.

“Having lots of genetic diversity within a species increases the chance that certain individuals contain the genetic background to adapt to a varied range of different environmental changes and diseases,” says Graham Etherington, a computational biologist at the Earlham Institute in Norwich, England, who was not involved with this research.

A shallower jungle fowl gene pool could also mean diminished resources for breeding better chickens. The genetics of wild relatives are sometimes used to bolster the disease or pest resistance of domesticated crop plants. Jungle fowl genomes could be similarly valuable for this reason.

“If this trend continues unabated, future human generations may only be able to access the entirety of ancestral genetic diversity of chickens in the form of museum specimens,” Rheindt says, which could hamper chicken breeding efforts using the wild fowl genes.

Some countries such as Singapore, Rheindt says, have started managing jungle fowl populations to reduce interbreeding with chickens.