Spiders may lack wings, but they aren’t confined to the ground. Under the right conditions, some spider species will climb to a high point, release silk strands to form a parachute, and float away on the breeze. Buoyed by air currents, they’ve been known to drift kilometers above Earth’s surface, and even to cross oceans to reach new habitats (SN: 2/4/17, p. 12).

Now, new research suggests air isn’t the only force behind this flight, called ballooning. Spiders can sense electrical charges in Earth’s atmosphere, and the forces exerted by these charges might be a cue for them to alight, researchers suggest July 5 in Current Biology. That invisible signal could help explain why spiders’ take-off timing seem a bit, well, flighty. Some days, arachnids balloon en masse; other days, they remain firmly grounded despite similar weather conditions.
Spiders with atmospheric aspirations do need a gentle breeze with speeds below around 11 kilometers per hour, past studies have shown. But those speeds alone shouldn’t be strong enough to get some of the larger species of ballooning spiders off the ground, says Erica Morley, a sensory biologist at the University of Bristol in England.
So scientists have long wondered if some other force might be involved: Perhaps electrical charges in Earth’s atmosphere push against the silken threads of airborne spiders’ silk streamers to help them stay fanned out in a parachute. These electric charges form an electric field that attracts or repels other charged objects or particles. It varies in strength, becoming stronger around objects such as leaves and branches on trees, and also fluctuating with meteorological conditions.
In the first experimental test of whether spiders can sense these electric charges, Morley and Bristol sensory biologist Daniel Robert blocked out naturally occurring electric fields in a lab. They then created an artificial one mimicking what would-be arthropod aerialists would experience, and placed teeny-tiny spiders from the Linyphiidae family into that faux field. Under the electric field, even with no breeze, the spiders perched on the tips of their legs, a ballerina-like behavior that precedes ballooning. When the researchers switched off the artificial electric field, the behavior (which scientists call the “tiptoe stance”) subsided.
Tiny hairs on the spiders’ bodies react to both moving air and an electric field’s presence, but differently, Morley found. The hairs stood on end as long as air was blowing on them. But when faced with an electric field, they stood on end most dramatically when the field was switched on and then gradually deflated to their resting position over about 30 seconds.

The study links the pre-ballooning tiptoeing behavior to the presence of an electric field, but actually taking off might require something more, suggests Moonsung Cho, an aerodynamics researcher at the Technical University of Berlin who wasn’t involved in the study. While some spiders in the study did incidentally float away, that liftoff behavior wasn’t actually measured.

And responding to electric fields probably isn’t the full story when it comes take-off timing: A different genus of spider, Xysticus, or ground crab spiders, appears to sense wind speed with its legs before going aloft, wiggling one spindly appendage around to sense moving air and determine whether wind conditions are favorable for lift-off, Cho’s team reported June 14 in PLOS Biology.

Neuroscientist Barbara Bendlin studies the brain as Alzheimer’s disease develops. When she goes home, she tries to leave her work in the lab. But one recent research project has crossed into her personal life: She now takes sleep much more seriously.

Bendlin works at the University of Wisconsin–Madison, home to the Wisconsin Registry for Alzheimer’s Prevention, a study of more than 1,500 people who were ages 40 to 65 when they signed up. Members of the registry did not have symptoms of dementia when they volunteered, but more than 70 percent had a family history of Alzheimer’s disease.

Since 2001, participants have been tested regularly for memory loss and other signs of the disease, such as the presence of amyloid-beta, a protein fragment that can clump into sticky plaques in the brain. Those plaques are a hallmark of Alzheimer’s, the most common form of dementia.

Each person also fills out lengthy questionnaires about their lives in the hopes that one day the information will offer clues to the disease. Among the inquiries: How tired are you?
Some answers to the sleep questions have been eye-opening. Bendlin and her colleagues identified 98 people from the registry who recorded their sleep quality and had brain scans. Those who slept badly — measured by such things as being tired during the day — tended to have more A-beta plaques visible on brain imaging, the researchers reported in 2015 in Neurobiology of Aging.

In a different subgroup of 101 people willing to have a spinal tap, poor sleep was associated with biological markers of Alzheimer’s in the spinal fluid, Bendlin’s team reported last year in Neurology. The markers included some related to A-beta plaques, as well as inflammation and the protein tau, which appears in higher levels in the brains of people with Alzheimer’s.

Bendlin’s studies are part of a modest but growing body of research suggesting that a sleep-deprived brain might be more vulnerable to Alzheimer’s disease. In animal studies, levels of plaque-forming A-beta plummet during sleep. Other research suggests that a snoozing brain runs the “clean cycle” to remove the day’s metabolic debris — notably A-beta — an action that might protect against the disease. Even one sleepless night appears to leave behind an excess of the troublesome protein fragment (SN Online: 7/10/17).

But while the new research is compelling, plenty of gaps remain. There’s not enough evidence yet to know the degree to which sleep might make a difference in the disease, and study results are not consistent.

A 2017 analysis combined results of 27 studies that looked at the relationship between sleep and cognitive problems, including Alzheimer’s. Overall, poor sleepers appeared to have about a 68 percent higher risk of these disorders than those who were rested, researchers reported last year in Sleep. That said, most studies have a chicken-and-egg problem. Alzheimer’s is known to cause difficulty sleeping. If Alzheimer’s both affects sleep and is affected by it, which comes first?

For now, the direction and the strength of the cause-and-effect arrow remain unclear. But approximately one-third of U.S. adults are considered sleep deprived (getting less than seven hours of sleep a night) and Alzheimer’s is expected to strike almost 14 million U.S. adults by 2050 (5.7 million have the disease today). The research has the potential to make a big difference.
It would be easier to understand sleep deprivation if scientists had a better handle on sleep itself. The brain appears to use sleep to consolidate and process memories (SN: 6/11/16, p. 15) and to catalog thoughts from the day. But that can’t be all. Even the simplest animals need to sleep. Flies and worms sleep.

But mammals appear to be particularly dependent on sleep — even if some, like elephants and giraffes, hardly nod off at all (SN: 4/1/17, p. 10). If rats are forced to stay awake, they die in about a month, sometimes within days.

And the bodies and brains of mice change when they are kept awake, says neurologist David Holtzman of Washington University School of Medicine in St. Louis. In one landmark experiment, Holtzman toyed with mice’s sleep right when the animals’ brain would normally begin to clear A-beta. Compared with well-rested mice, sleep-deprived animals developed more than two times as many amyloid plaques over about a month, Holtzman says.
He thinks Alzheimer’s disease is a kind of garbage collection problem. As nerve cells, or neurons, take care of business, they tend to leave their trash lying around. They throw away A-beta, which is a leftover remnant of a larger protein that is thought to form connections between neurons in the developing brain, but whose role in adults is still being studied. The body usually clears away A-beta.

But sometimes, especially when cheated on sleep, the brain doesn’t get the chance to mop up all the A-beta that the neurons produce, according to a developing consensus. A-beta starts to collect in the small seams between cells of the brain, like litter in the gutter. If A-beta piles up too much, it can accumulate into plaques that are thought to eventually lead to other problems such as inflammation and the buildup of tau, which appears to destroy neurons and lead to Alzheimer’s disease.

About a decade ago, Holtzman wanted to know if levels of A-beta in the fluid that bathes neurons fluctuated as mice ate, exercised, slept and otherwise did what mice do. It seemed like a run-of-the-mill question. To Holtzman’s surprise, time of day mattered — a lot. A-beta levels were highest when the animals were awake but fell when the mice were sleeping (SN: 10/24/09, p. 11).

“We just stumbled across this,” Holtzman says. Still, it wasn’t clear whether the difference was related to the hour, or to sleep itself. So Holtzman and colleagues designed an experiment in which they used a drug to force mice to stay awake or fall asleep. Sure enough, the A-beta levels in the brain-bathing fluid rose and fell with sleep, regardless of the time on the clock.

A-beta levels in deeply sleeping versus wide-awake mice differed by about 25 percent. That may not sound like a dramatic drop, but over the long term, “it definitely will influence the probability [that A-beta] will aggregate to form amyloid plaques,” Holtzman says.

The study turned conventional thinking on its head: Perhaps Alzheimer’s doesn’t just make it hard to sleep. Perhaps interrupted sleep drives the development of Alzheimer’s itself.

Published in Science in 2009, the paper triggered a flood of research into sleep and Alzheimer’s. While the initial experiment found that the condition worsens the longer animals are awake, research since then has found that the reverse is true, too, at least in flies and mice.

Using fruit flies genetically programmed to mimic the neurological damage of Alzheimer’s disease, a team led by researchers at Washington University School of Medicine reversed the cognitive problems of the disease by simply forcing the flies to sleep (SN: 5/16/15, p. 13).

Researchers from Germany and Israel reported in 2015 in Nature Neuroscience that slow-wave sleep — the deep sleep that occupies the brain most during a long snooze and is thought to be involved in memory storage — was disrupted in mice that had A-beta deposits in their brains. When the mice were given low doses of a sleep-inducing drug, the animals slept more soundly and improved their memory and ability to navigate a water maze.

Gray matters
Even with these studies in lab animals indicating that loss of sleep accelerates Alzheimer’s, researchers still hesitate to say the same is true in people. There’s too little data. Human studies are harder and more complicated to do. One big hurdle: The brain changes in humans that lead to Alzheimer’s build up over decades. And you can’t do a controlled experiment in people that forces half of the study’s volunteers to endure years of sleep deprivation.

Plus the nagging chicken-and-egg problem is hard to get around, although a study published in June in JAMA Neurology tried. Researchers from the Mayo Clinic in Rochester, Minn., examined the medical records of 283 people older than 70. None had dementia when they enrolled in the Mayo Clinic Study of Aging. At the study’s start, participants answered questions about their sleep quality and received brain scans looking for plaque deposits.

People who reported excessive daytime sleepiness — a telltale sign of fitful sleep — had more plaques in their brains to start with. When checked again about two years later, those same people showed a more rapid accumulation than people who slept soundly.

Other scientists have used brain scans to measure what happens to A-beta in people’s brains after a sleepless night. Researchers from the National Institutes of Health and colleagues completed a study involving 20 healthy people who had a brain scan while rested and then again after they were forced to stay awake for 31 hours.

Nora Volkow, head of the National Institute on Drug Abuse in Bethesda, Md., led the study. She is interested in sleep’s potential connections to dementia because people with drug addiction have massive disruptions of sleep. For the study, the researchers injected people with a compound that latches onto A-beta and makes it visible under a PET scanner.

The sleep-deprived brains showed an increase in A-beta accumulation that was about 5 percent higher in two areas of the brain that are often damaged early in Alzheimer’s: the thalamus and hippocampus. Other regions had lesser buildup.

“I was surprised that it was actually so large,” says study coauthor Ehsan Shokri-Kojori, now at the National Institute on Alcohol Abuse and Alcoholism. “Five percent from one night of sleep deprivation is far from trivial.” And while the brain can likely recover with a good night’s sleep, the question is: What happens when sleep deprivation is a pattern night after night, year after year?

“It does highlight that sleep is indispensable for proper brain function,” Volkow says. “What we have to question is what happens when you are consistently sleep deprived.” The study was published April 24 in the Proceedings of the National Academy of Sciences.
As tantalizing as studies like this may seem, there are still inconsistencies that scientists are trying to resolve. Consider a study published in May in Sleep from a team of Swedish and British researchers. They set out to measure levels of A-beta in cerebrospinal fluid and markers of neuron injury in 13 volunteers, sleep deprived and not.

The first measurements took place after five nights of sound sleep. Then participants were cut back to four hours of sleep a night, for five nights. Four participants even lasted eight days with only four hours of nightly sleep. After good sleep versus very little, the measurements did not show the expected differences.

“That was surprising,” says Henrik Zetterberg of the University Gothenburg in Sweden. Given the previous studies, including his own, “I would have expected a change.”

He notes, however, that the study participants were all healthy people in their 20s and 30s. Their youthful brains might cope with sleep deprivation more readily than those in middle age and older. But that’s just a hypothesis. “It shows why we have to do further research,” he says.

Rinse cycle
Questions could be better answered if scientists could find a mechanism to explain how sleepless nights might exacerbate Alzheimer’s. In 2013, scientists revealed an important clue.

The lymphatic system flows through the body’s tissues to pick up waste and carry it away. All lymphatic vessels run to the liver, the body’s recycling plant for used proteins from each organ’s operation. But the lymphatic system doesn’t reach the brain.

“I found it weird because the brain is our most precious organ — why should it be the only organ that recycles its own proteins?” asks Maiken Nedergaard, a neuroscientist at the University of Rochester in New York. Maybe, she thought, the brain has “a hidden lymphatic system.”

Nedergaard and colleagues decided to measure cerebrospinal fluid throughout the brain. When mice were awake, there appeared to be little circulation of fluid in the brain. Then the team examined sleeping mice. “You take mice and train them to be quiet under a microscope,” Nedergaard says. “The mice after a couple of days feel very calm. Especially if you do it during the daytime when they are supposed to be sleeping, and they are warm and you give them sugar water. They’re not afraid.”
Slumbering stream
Flow of cerebrospinal fluid in a mouse’s brain is much higher during sleep (left, red) than when the animal is awake (right, green).

The day of the experiment, the scientists made a hole in the mice’s skulls, placed a cover over it and injected a dye to measure cerebrospinal fluid in the brain. During sleep, the spaces between the brain cells widened by about 60 percent and allowed more fluid to wash through, taking the metabolic debris, including A-beta, with it.

“It’s like the dishwasher turned on,” Nedergaard says. She named this phenomenon the “glymphatic system” because it appears to be controlled by glial cells, brain cells that help insulate neurons and perform much of the brain’s routine maintenance work (SN: 8/22/15, p. 18).

Similar observations of cerebrospinal fluid circulation have been carried out in people, but with less invasive ways of measuring. In one, researchers from Oslo University Hospital, Rikshospitalet compared 15 patients who had a condition called normal pressure hydrocephalus, a kind of dementia caused by buildup of cerebrospinal fluid in the cavities of the brain, with eight people who didn’t have the condition.

The researchers used a tracer for cerebrospinal fluid and magnetic resonance imaging to measure the flow over 24 hours. Immediately after a night’s sleep, cerebrospinal fluid had drained in healthy people but lingered in the patients with dementia, the researchers reported in Brain in 2017.
Don’t snooze, you lose?
The central question — the one that doctors really want to answer — is whether better sleep could treat or even prevent Alzheimer’s. To try to figure this out, Bendlin and her Wisconsin colleagues are now studying people with sleep apnea. People with that condition stop breathing during the night, which wakes them up and makes for a lousy night’s sleep. A machine called a CPAP, short for continuous positive airway pressure, treats the condition.

“Once people start treatment, what might we see in the brain? Is there a beneficial effect of CPAP on markers of Alzheimer’s?” Bendlin wonders. “I think that’s a big question because the implications are so large.”

A study reported in Neurology in 2015 offers a reason to think CPAP might help. Using data from almost 2,500 people in the Alzheimer’s Disease Neuroimaging Initiative, researchers at the New York University School of Medicine found that people with sleep disorders like obstructive sleep apnea showed signs of mild cognitive problems and Alzheimer’s disease at younger ages than those who did not. But for those who used CPAP, onset of mild cognitive problems was delayed.

“If we find out that sleep problems contribute to brain amyloid — what that really says is there may be a window to intervene,” Bendlin says. And the solution — more attention to sleep — is one prescription with no side effects.

A new computer program works smarter, not harder, to solve problems faster than its predecessors.

The algorithm is designed to find the best solution to a given problem among all possible options. Whereas other computer programs winnow down the possibilities one at a time, the new program — presented July 12 at the International Conference on Machine Learning in Stockholm — rules out many choices at once.

For instance, imagine a computer is assigned to compile movie recommendations based on a particular film. The ideal recommendation list would include suggestions that are both similar to the original flick — say, in the same genre — yet different enough from each other to give the viewer a variety of choice. A traditional recommendation system would pore over an entire movie library to find films that best met those criteria and add films to its roster of recommendations one by one, a relatively slow and tedious process.
By contrast, the new program starts by randomly picking a bunch of movies from the library. Among that sample, the system keeps the movies that strike the best balance between relevance to the original film and diversity, and discards the rest. From that smaller pool, the algorithm again chooses films at random and keeps only the best of the bunch. That strategy helps the algorithm build its rec list far faster.

The new algorithm, built by Harvard University computer scientists Yaron Singer and Eric Balkanski, compiled movie suggestions more than 10 times as fast as a standard recommender system. In another trial, it devised optimal routes for cabs in New York City about six times as fast as a conventional automated dispatcher.

This program could also speed up data processing for everything from drug discovery to social media analytics and analyses of genetic data (SN Online: 7/15/15).

Keeping a tight lid on blood pressure isn’t just good for the heart. It may also help the brain.

People given intensive drug treatment for high blood pressure were less likely to develop an early form of memory loss, according to preliminary results from a major clinical trial. This approach reduced the rate of early memory loss, called mild cognitive impairment, by around 19 percent, compared with people who received less aggressive treatment.

And the intensely treated group developed fewer white matter lesions over time, researchers reported July 25 at the Alzheimer’s Association International Conference in Chicago. White matter lesions, which are associated with dementia, are thought to be caused by blood vessel injuries in white matter, the part of the brain that contains nerve fibers.
The brain research is part of SPRINT, the Systolic Blood Pressure Intervention Trial involving more than 9,300 participants. Some received intensive treatment aimed at lowering their systolic blood pressure — the pressure on artery walls when the heart beats — below 120 millimeters of mercury; others got standard treatment to bring it below 140.

The trial had already reported that participants who received the intensive treatment dropped their risk of heart attacks and other cardiovascular problems by 25 percent, compared with the standard group (SN Online: 11/9/2015). The results were the basis for revamped blood pressure guidelines, released last year (SN: 12/9/17, p. 13).

Dubbed SPRINT-MIND, the brain research set out to measure whether aggressively controlling blood pressure benefits the brain along with the heart. Observational studies have shown that people with lower blood pressure have a lower risk of developing dementia, says Jeff Williamson, a geriatrician at Wake Forest School of Medicine in Winston-Salem, N.C.
Using memory tests, experts assessed the trial participants for probable dementia (people unable to perform daily activities independently), early memory loss (people with some difficulty functioning, but still independent) or no impairment. More than 8,600 of the participants completed an assessment up until June 2018; their average age was about 68 years old.

Fewer people in the intensely treated group had the early memory loss, which is often a precursor to dementia, Williamson says. And fewer had probable dementia as well, although the results were not statistically significant. The trial was ended early, in 2015, due to the compelling cardiovascular benefits, so participants’ blood pressure was medically managed for only two to three years. “That’s an encouraging message,” Williamson says. “It doesn’t take but just a few years to see this effect.”

The SPRINT-MIND trial also looked at white matter lesions. These injuries in the brain are a consequence of aging, but they are also associated with hypertension, says neuroradiologist Ilya Nasrallah of the University of Pennsylvania. Previous work has found that white matter lesions increase the risk of dementia in people ages 60 and older.

About 450 participants had MRI brain scans at the start of the trial and roughly four years later. The volume of white matter lesions increased by 0.28 cubic centimeters over that time in the intensive treatment group, compared with 0.92 cubic centimeters in the standard treatment group. With intense blood pressure treatment, Nasrallah says, “we could slow progression of white matter lesions.”

But there is evidence that the relationship between blood pressure and brain health may change with advancing age, notes cognitive neurologist Zoe Arvanitakis of Rush University Medical Center in Chicago, who was not involved with the trial.

In adults 75 and older, past work has found that low diastolic blood pressure — the pressure on arteries when the heart rests between beats — increases the risk of dementia. The age at which people are at high risk for dementia is older than the average age of those in SPRINT, Arvanitakis says. “We really need to study this question in older persons as well.”

Neurologist and neuroscientist Costantino Iadecola of Weill Cornell Medicine in New York City says that, in general, the study shows that lowering blood pressure closer to 120 has beneficial effects on the brain. The problem is that in midlife, when people are 40 to 60 years old, “there is no question that high blood pressure is bad for you,” but that’s not true for those 80 and above, he says. Older people may need higher blood pressure to get enough blood flow to the brain.

Still, the study “is a piece of good news in an otherwise grim landscape” regarding dementia, Iadecola says, because it suggests “you can make the brain better if you take care of your blood pressure.”

A Mars orbiter has detected a wide lake of liquid water hidden below the planet’s southern ice sheets. There have been much-debated hints of tiny, ephemeral amounts of water on Mars before. But if confirmed, this lake marks the first discovery of a long-lasting cache of the liquid.

“This is potentially a really big deal,” says planetary scientist Briony Horgan of Purdue University in West Lafayette, Ind. “It’s another type of habitat in which life could be living on Mars today.”
The lake is about 20 kilometers across, planetary scientist Roberto Orosei of the National Institute of Astrophysics in Bologna, Italy and his colleagues report online July 25 in Science — but the water is buried beneath 1.5 kilometers of solid ice.

Orosei and colleagues spotted the lake by combining more than three years of observations from the European Space Agency’s orbiting Mars Express spacecraft. The craft’s MARSIS instrument, which stands for Mars Advanced Radar for Subsurface and Ionosphere Sounding, aimed radar waves at the planet to probe beneath its surface.
As those waves passed through the ice, they bounced off different materials embedded in the glaciers. The brightness of the reflection tells scientists about the material doing the reflecting — liquid water makes a brighter echo than either ice or rock.

Combining 29 radar observations taken from May 2012 to December 2015, MARSIS revealed a bright spot in the ice layers near Mars’ south pole, surrounded by much less reflective areas. Orosei and colleagues considered other explanations for the bright spot, such as radar bouncing off a hypothetical layer of carbon dioxide ice at the top of the sheet, but decided those options either wouldn’t produce the same radar signal or were too contrived to be physically likely.

That left one option: A lake of liquid water. Similar lakes beneath the ice in Antarctica and Greenland have been discovered in the same way (SN: 9/7/13, p. 26).

“On Earth, nobody would have been surprised to conclude that this was water,” Orosei says. “But to demonstrate the same on Mars was much more complicated.”

The lake is probably not pure water — temperatures at the bottom of the ice sheet are around –68° Celsius, and pure water would freeze there, even under the pressure of so much ice. But a lot of salt dissolved in the water could lower the freezing point. Salts of sodium, magnesium and calcium have been found elsewhere on Mars, and may be helping to keep this lake liquid (SN: 4/11/09, p. 12). The pool could also be more mud than water, but that could still be a habitable environment, Horgan says.

Previously, scientists have discovered extensive solid water ice sheets under the Martian dirt (SN Online: 1/11/18). There were also hints that liquid water flowed down cliff walls (SN: 10/31/15, p. 17), but those may turn out to be tiny dry avalanches. The Phoenix lander saw what looked like frozen water droplets at its site near the north pole in 2008, but that water may have been melted by the lander itself (SN Online: 9/9/10).

“If this [lake] is confirmed, it’s a substantial change in our understanding of the present-day habitability of Mars,” says Lisa Pratt, NASA’s planetary protection officer.

Though the newly discovered lake’s depth is unclear, its volume still dwarfs any previous signs of liquid water on Mars, Orosei says. The lake has to be at least 10 centimeters deep for MARSIS to have noticed it. That means it could contain at least 10 billion liters of liquid water.

“That’s big,” Horgan says. “When we’ve talked about water in other places, it’s in dribs and drabs.”

Under-ice lakes on Mars were first suggested in 1987, and the MARSIS team has been searching since Mars Express began orbiting the Red Planet in 2003. It took the team more than a decade to collect enough data to convince themselves the lake was real.

For the first several years of observations, limitations in the spacecraft’s onboard computer forced the team to average hundreds of radar pulses together before sending the data back to Earth. That strategy sometimes cancelled out the lake’s reflections, Orosei says — on some orbits, the bright spot was visible, on others, it wasn’t.

In the early 2010s, the team switched to a new technique that let them store the data and send it back to Earth more slowly. Then in August 2015, months before the end of the observing campaign, the experiment’s principal investigator, Giovanni Picardi of the University of Rome Sapienza, died unexpectedly.

“It was incredibly sad,” Orosei says. “We had all the data, but we had no leadership. The team was in disarray.”

Finally discovering the lake is “a testament to perseverance and longevity,” says planetary scientist Isaac Smith of the Planetary Science Institute, who is based in Lakewood, Colo. “Long after everyone else gave up looking, this team kept looking.”

But there is still room for doubt, says Smith, who works on a different radar experiment on NASA’s Mars Reconnaissance Orbiter that has seen no sign of the lake, even in CT scan–like 3-D views of the poles. It could be that MRO’s radar is scattering off the ice in a different way, or that the wavelengths it uses don’t penetrate as deep into the ice. The MRO team will look again, and will also try to create a 3-D view from the MARSIS data. Having a specific spot to aim for is helpful, he says.

“I expect there will be debate,” Smith says. “They’ve done their homework. This paper is well earned. But we should do some more follow-up.”

Stonehenge attracted the dead from far beyond its location in southern England.

A new analysis of cremated human remains interred at the iconic site between around 5,000 and 4,400 years ago provides the first glimpse of who was buried there. Some were outsiders who probably spent the last decade or so of their lives in what’s now West Wales, more than 200 kilometers west of Stonehenge, researchers report August 2 in Scientific Reports.

West Wales was the source of rocks known as bluestones used in early stages of constructing Stonehenge. Bluestones are smaller than the ancient monument’s massive sandstone boulders.
The new investigation “adds detail to a previously rather shaky framework” of archaeological finds suggesting that links existed among ancient societies across southern England and Wales, says archaeologist Timothy Darvill of Bournemouth University in Poole, England, who was not involved in the research.

Geographic origins of cremated remains at the site had previously eluded scientists. In the new study, bioarchaeologist Christophe Snoeck of Vrije Universiteit Brussel in Belgium and colleagues analyzed two forms of the element strontium in human skull fragments that were previously found among cremated remains at Stonehenge to narrow down individuals’ origins. Signature levels of these strontium types characterize rock formations and soil in different regions. Humans and other animals incorporate strontium into their bones and teeth by eating plants.
Snoeck demonstrated several years ago that, rather than absorbing strontium from surrounding soil like unburned bone, pieces of cremated bone retain a strontium signal from around the last 10 years of a person’s life. Of 25 cremated people whose bones were studied, 10 individuals spent their last decade in West Wales or near there, the researchers found. The rest were locals.
“Our results show that it was not just bluestones but people, or in some cases perhaps just their cremated remains, that came to Stonehenge in its early phases,” says coauthor Rick Schulting, an archaeologist at the University of Oxford.

Stonehenge served as a cemetery for at least 500 years, beginning around 5,000 years ago (SN: 6/21/08, p. 13). Excavations at Stonehenge between 1919 and 1926 recovered cremated remains of up to 58 individuals that had been placed in 56 pits. Researchers reburied these finds in 1935. Archaeologist and study coauthor Mike Parker Pearson of University College London led a team that in 2008 re-excavated remnants of the 25 individuals analyzed in the new study.
Nonlocal people buried at Stonehenge were cremated before being transported to the ancient site, Snoeck’s group suspects. Levels of two forms of carbon absorbed into the bones during cremation indicate that funeral pyres consisted of trees from dense woods such as those in Wales. A different carbon makeup characterizes trees from relatively open landscapes, as in southern England. The extent of contacts between communities in the two regions is unknown. One reason: Cremation destroys tooth enamel, which preserves a strontium record of childhood diet. As a result, investigators can’t determine whether nonlocal people buried at Stonehenge grew up in West Wales or elsewhere.

For now, the best bet is that nonlocal people buried at Stonehenge around 5,000 years ago spent their final years in western Britain, possibly West Wales, says archaeologist Alasdair Whittle of Cardiff University in Wales. Archaeological finds from that time link inhabitants of the Orkney Islands off Scotland’s northeast coast to communities in mainland Britain and probably continental Europe, boosting the plausibility of long-distance contacts between western Britain and Stonehenge, Whittle adds.

Archaeologists also have discovered cultural ties between southern England and France’s northwestern Brittany region dating to as early as around 5,000 years ago, Darvill says. That means outsiders could have come from other places. Snoeck’s group should compare strontium signatures typical of Brittany folk to those of people buried at Stonehenge, he suggests.

The extinction event that wiped out all nonbird dinosaurs about 66 million years ago also shook up shark evolution.

Fossilized shark teeth show that the extinction marked a shift in the relative fates of two groups of sharks. Apex predators called lamniformes, which include modern great white sharks, dominated the oceans before the event, which took place at the end of the Cretaceous Period. But afterward, midlevel predator sharks called carcharhiniformes came to dominate the waters — as they still do today, researchers report August 2 in Current Biology.
Paleontologist Mohamad Bazzi of Uppsala University in Sweden and colleagues examined the shapes of nearly 600 shark teeth dating from 72 million to 56 million years ago. Unlike their cartilaginous skeletons, sharks’ teeth, which the fish shed throughout their lives, are well preserved in the fossil record, Bazzi says. By looking at patterns in tooth shape variation — the height of the crown or the breadth of the tooth — scientists can measure trends in shark diversity. After the extinction event, lamniform sharks that had a particular tooth shape — low-crowned and triangular — appeared to decline, while carcharhiniform sharks with the same low-crowned tooth shape proliferated.

The extinction “is one of the more transformative events in shark evolution,” Bazzi says. Today, there are only 15 known species of lamniformes, but hundreds of carcharhiniformes, including hammerheads and lemon sharks.

It’s difficult to know how the event caused the shift, but one possibility is that the extinction affected the sharks’ preferred food sources. Modern great whites, for example, eat everything from cephalopods to seals; ancient lamniformes may have had a similarly varied diet and experienced a loss of primary food sources such as marine reptiles following the extinction. But the rapid increase in small bony fish after the event may have given a boost to the smaller carchariniform predators, such as houndsharks.

The first new treatment in 60 years for a particularly stubborn kind of malaria is raising hopes that it might help eradicate the disease, even though the treatment can cause a dangerous side effect.

Called tafenoquine, the drug targets the parasite that causes relapsing malaria. Plasmodium vivax infects an estimated 8.5 million people, mainly in Asia and Latin America. Each time infected people have a malaria relapse, the parasite returns to their bloodstream, allowing them to transmit the infection if a mosquito bites them again. Tafenoquine was approved as a treatment in July by the U.S. Food and Drug Administration and is under consideration as a preventative medication, too.
“This is a game changer because we’ve really been struggling with eliminating [P.] vivax,” says malaria physician Ric Price from the Menzies School of Health Research in Darwin, Australia.

The FDA’s action is expected to spur other countries where relapsing malaria is more prevalent to approve the drug as well. Companies are also working to develop speedy, low-cost tests that can identify people with a genetic deficiency who may risk getting a kind of anemia from the new drug. This test is essential for putting the drug to use in rural areas where rates of both P. vivax and this deficiency can be high.

Like its deadlier cousin P. falciparum, P. vivax is spread by the Anopheles mosquito and causes chills, a cyclical fever and joint aches (SN: 3/18/17, p. 10). Unlike P. falciparum, once inside the body, P. vivax can stay dormant in the liver for weeks or months before flaring up again and again.

Tafenoquine (which will be marketed in the United States as Krintafel) is designed to prevent these relapses. It is similar to an older drug called primaquine, but it is taken in two 150-milligram doses a few hours apart, instead of daily for two weeks. In clinical trials, that dosage, paired with acute malaria medication chloroquine, prevented 70 percent of malaria relapses.
With its compressed dosing schedule, patients prescribed tafenoquine are more likely than those on primaquine to complete the treatment, preventing more relapses and problems with drug resistance.

But tafenoquine’s biggest selling point is also a weakness. Both primaquine and tafenoquine can cause a dangerous side effect in people with glucose-6-phosphate dehydrogenase, or G6PD, deficiency, an abnormality on the X chromosome that affects 400 million people worldwide. When people who have G6PD deficiency take these medications, they are at a higher risk for hemolytic anemia, the destruction of red blood cells.

Tafenoquine’s long-lasting formula makes it harder for the body to clear it out, which could potentially lead to life-threatening damage to red blood cells and severe anemia. “Once it’s in your body, it stays in your body,” says Nick White, a physician and malaria expert at the Mahidol Oxford Tropical Medicine Research Unit at the University of Oxford in Bangkok.

Tests to determine which patients have G6PD deficiency are not widely available, particularly in developing countries such as those in Asia and South America where relapsing malaria is endemic. “The test exists,” says Gonzalo Domingo, a scientific director at PATH, a nonprofit global health organization in Seattle, “but it is quite complicated, and it requires quite complicated laboratory facilities.”

PATH funds companies that are developing a new version of the test for use in rural areas. Field trials of a prototype test that can be performed in two minutes with just a finger prick are under way in Ethiopia, Brazil and India. People with relapsing malaria who test positive for G6PD deficiency instead take a low-dose, eight-week treatment of primaquine that’s less likely to cause side effects.

“It’s a great tool,” Domingo says of the new G6PD deficiency test. “It provides people access to the drug safely.”

A gene that helps mammals break down certain toxic chemicals appears to be faulty in marine mammals — potentially leaving manatees, dolphins and other warm-blooded water dwellers more sensitive to dangerous pesticides.

The gene, PON1, carries instructions for making a protein that interacts with fatty acids ingested with food. But that protein has taken on another role in recent decades: breaking down toxic chemicals found in a popular class of pesticides called organophosphates. As the chemicals drain from agricultural fields, they can poison waterways and coastal areas and harm wildlife, says Wynn Meyer, an evolutionary geneticist at the University of Pittsburgh.
An inspection of the genetic instructions of 53 land mammal species found the gene intact. But in five marine mammal species, PON1 was riddled with mutations that made it useless, Meyer and colleagues report in the Aug. 10 Science. The gene became defunct about 64 million to 21 million years ago, possibly due to dietary or behavioral changes related to marine mammal ancestors’ move from land to sea, the researchers say.

The team also gauged the rate at which two organophosphate chemicals — chlorpyrifos oxon and diazoxon — broke down in blood samples from five land mammal species and six marine or semiaquatic mammal species. While blood from the terrestrial species, including sheep, goats and ferrets, showed a decrease in toxic molecules over time, the marine species’ blood showed almost no change. Mice genetically engineered to lack the gene couldn’t break down the chemicals either.
A nonfunctional PON1 doesn’t necessarily mean marine mammals are helpless against organophosphates, says environmental toxicologist Andrew Whitehead at the University of California, Davis who was not involved in the work. The animals may have other defense mechanisms, but in this study, “they aren’t stepping up to the plate to metabolize these organophosphates,” he says.
It’s unclear if organophosphates build up in marine mammals’ bodies in a way similar to DDT, a type of pesticide that doesn’t break down easily in the environment. DDT, which is banned in dozens of countries, can accumulate in marine mammals’ tissues and cause nervous system damage and birth defects (SN Online: 1/19/16).

What’s more, “even though organophosphates don’t stick around as long in the environment as DDT, there’s persistent input,” Whitehead says. The chemicals are often used on crops and to kill mosquitoes and other pests.

The researchers plan to collect blood samples from dolphins and manatees in coastal areas suffused with agricultural runoff, says study coauthor Nathan Clark, an evolutionary biologist also at the University of Pittsburgh. That could help scientists monitor if the animals have been exposed to the pesticides and if that corresponds with levels of the chemicals in the environment, he says.

Rogue nations that want to hide nuclear weapons tests may one day be thwarted by antineutrinos.

Atomic blasts emit immense numbers of the lightweight subatomic particles, which can travel long distances through the Earth. In general, the particles — the antimatter twins of neutrinos — are notoriously difficult to spot. But a large antineutrino detector located within a few hundred kilometers of a powerful nuclear explosion could glimpse a handful of the particles, scientists report in the August Physical Review Applied.
An antineutrino detector wouldn’t spot an explosion solely on its own, but would use seismic activity picked up by existing sensors to trigger a search for particles arriving from a suspected blast. It’s “a very smart and clever idea,” says physicist Patrick Huber of Virginia Tech in Blacksburg.

A global network of sensors already gathers detailed information about nuclear explosions by monitoring for telltale seismic activity and radioactive isotopes. In recent years, those sensors have revealed details of North Korean nuclear tests performed underground (SN: 8/5/17, p. 18).

But if those sensors were unable to confirm that a nuclear explosion occurred, spotting antineutrinos would eliminate doubt, says study coauthor and physicist Adam Bernstein of Lawrence Livermore National Laboratory in California. “If you see a burst of antineutrinos, there’s really no other way you could have gotten that,” he says, aside from an exploding star in the Milky Way (SN: 2/18/17, p. 24). Those stellar bursts are rare events unlikely to coincide with a seismic signature.

And while stealthy bomb makers might be able to contain an explosion’s radioactive isotopes or mask some of its seismic signals, there’s no way to stop antineutrinos from escaping. Neutrinos could also provide information about how powerful the explosion was and what type of nuclear weapon was used.
None of the existing antineutrino detectors, however, are big enough and in the right location to monitor North Korea. One of the biggest is the Super-Kamiokande detector, located in a mine in Hida, Japan. It’s filled with 50,000 tons of water and lined with sensors that detect light produced when antineutrinos interact in the water. If located within about 100 kilometers of a nuclear test site, a detector of this size could likely spot a 250-kiloton nuclear fission explosion.

A detector about 10 times bigger could spot such an explosion several hundred kilometers away. But building such large detectors wouldn’t be easy. “It’s not the kind of thing that’s going to be the go-to method for monitoring nuclear testing,” says physicist Kate Scholberg of Duke University.

Scientists are planning a beefed-up antineutrino experiment of that size called Hyper-Kamiokande, which would consist of two detectors, one in Japan and the other in South Korea. Hyper-Kamiokande’s main purpose is to study the physics of neutrinos. But, says study coauthor Rachel Carr, a physicist at MIT, the proposed South Korean detector is “actually big enough that it would possibly detect a few antineutrinos from a North Korean test.”