In the early stages of Alzheimer’s disease, an overzealous set of proteins and cells begins to chew away at the brain’s nerve cell connections, a study in mice suggests.

That finding, described March 31 in Science, adds to a growing body of research that implicates excessive synaptic pruning, a process that shapes the young brain by culling unused connections, with disorders later in life. The new work pins the loss of nerve cell–connecting synapses on particular immune system molecules and a notorious Alzheimer’s-linked protein.
By uniting these multiple strands of evidence, the study may help explain the earliest steps in Alzheimer’s march of neural destruction. “No one has put it together in quite this way,” says neuropathologist John Trojanowski. If the same process happens in humans, the new results may point to ways to slow or stop Alzheimer’s, says Trojanowski, of the University of Pennsylvania’s medical school.

A curious observation led to this new view of neural whittling. A protein called C1q was packed around synapses in the brains of young mice genetically engineered to show signs of Alzheimer’s. And C1q was most abundant in brain areas known to suffer synapse losses as Alzheimer’s takes hold.

C1q is a member of the complement cascade, a group of immune system proteins that calls in microglia cells to gobble up synapses or cells. This pruning is essential as the brain develops. But these neural gardeners seem to spring back into action in the early stages of Alzheimer’s, neuroscientist Beth Stevens of Boston Children’s Hospital and Harvard University and colleagues found. And that reactivation seems to be helped along by the Alzheimer’s-related protein amyloid-beta.

In the brains of mice that weren’t genetically engineered, injections of oligomeric A-beta, the form thought to be the most dangerous, caused C1q levels to rise. Along with this increase, synapses got destroyed, the team found. But A-beta injections didn’t harm synapses in mice lacking C1q, showing that C1q and A-beta are both needed for excessive pruning. How the two proteins exactly work together isn’t clear, Stevens says, but “they are definitely there at the right time and the right place.”

Complement proteins and microglia are known to be active in late-stage Alzheimer’s, when the inflamed brain is packed with sticky gobs of A-beta. But the new results suggest that the synapse-pruning pathway is active much earlier in the disease process, long before A-beta plaques form. “The story is extremely compelling and tight in Alzheimer’s mouse models,” says neurologist Scott Small of Columbia University.
There are reasons to think that a similar process happens in people. Autopsy studies by neurobiologist Stephen Scheff of the University of Kentucky in Lexington and colleagues, for instance, have turned up fewer synapses in the brains of people with mild cognitive impairment — thought to be an early stage of Alzheimer’s. The cause of that synapse loss could certainly be explained by changes in complement proteins or microglia, Scheff says.

Any therapy that would target this pruning process would first depend on identifying people at risk. And so far, there are no good tests to spot excessive oligomeric A-beta in the brain, says neurologist Sam Gandy of Mount Sinai Medical Center in New York City. “Oligomers are invisible,” he says.

But if screening methods are developed, then the prospect of stopping Alzheimer’s by stopping synapse loss is appealing, Small says. A drug that could prevent C1q or its conspirators from targeting synapses for destruction might halt the damage, for instance. “It’s easier to cure a sick cell than a dead cell,” he says.

Overactive synaptic pruning may be behind other brain disorders, Stevens suspects. She and her colleagues recently implicated a different complement cascade protein in schizophrenia (SN: 2/20/16, p. 7). “This may be a pathway that is dysregulated and playing a role in synapse loss in a host of neurological diseases, not just one,” she says. Stevens and several coauthors are involved with a company that is developing a drug to block C1q.

Where it rains, it rumbles. Rainwater and snowmelt help fuel intense earthquakes along a New Zealand tectonic fault, new research suggests.

Tracing the source of water flowing through New Zealand’s Alpine Fault shows that more than 99 percent of it originated from precipitation, researchers report April 19 in Earth and Planetary Science Letters. Scientists knew that underground fluids help trigger quakes, but the origins of these fluids have been uncertain. In this case, the nearby Southern Alps concentrate rainfall and meltwater on top of the Alpine Fault while the fault itself serves as an impermeable dam that traps the water.
The fault “essentially [is] promoting its own large fluid pressures that can lead to earthquakes,” says study coauthor Catriona Menzies, a geologist at the University of Southampton in England. Identifying the fluid source will help scientists better predict the fault’s seismic cycle, she says.

New Zealand sits on the boundary where the Australian and Pacific tectonic plates collide. This collision generates a powerful earthquake along the Alpine Fault around once every 330 years, with the most recent temblor in 1717; it also gradually formed the Southern Alps as the two plates scrunched upward. Moist air condenses on its way up and over the mountains, causing torrential rainfall that typically exceeds 10 meters annually. Menzies and colleagues wondered how much rainwater makes its way to the fault. Fluids within a fault help induce quakes by altering the strength of rock and by counteracting the forces that hold two sides of a fault together (SN: 7/11/15, p. 10).
Water divulges its origins in several ways. The researchers looked at water-deposited minerals in rocks, the relative abundance of helium in nearby hot springs and the various oxygen and hydrogen isotopes that made up the water — all fingerprints of the water’s source. Even though only about 0.02 to 0.05 percent of rainwater makes it to the fault’s depth, the work revealed that more water came from precipitation than from all other sources, such as water released from surrounding rocks and the underlying mantle. The 3-kilometer-tall Southern Alps may even serve as a water tower that boosts water pressure by heightening the stack of groundwater that sits on top of the fault.

While local geography makes the Alpine Fault unique, the new work provides a template for studying fluids in other earthquake-prone areas such as the recently active Japanese fault, says Patrick Fulton, a geophysicist at Texas A&M University in College Station.

Growth hormone mapped — Discovery of the complete chemical structure of the human growth hormone has been reported…. The discovery marks a major advance toward understanding how the powerful growth-promoting substance works and increases the chances for its eventual synthesis in the laboratory…. Some 5,000 fresh human pituitary glands were required to achieve the results.
— Science News, May 21, 1966

Update
In 1979, researchers produced a synthetic human growth hormone in the lab, using bacteria equipped with human hormone genes. Six years later, the synthetic growth hormone was approved for medical use; distribution of growth hormone collected from human pituitary glands had been halted after infected product was linked to Creutzfeldt-Jakob disease, a fatal brain-wasting disorder. Today, doctors use synthetic growth hormone to treat growth hormone deficiency, which can stunt growth in children. Because synthetic growth hormone can build muscle and trim body fat, it is prohibited as a doping agent by many sports organizations.

Nearly 300 pregnant women in the United States show laboratory evidence of Zika virus infection.

The U.S. Centers for Disease Control and Prevention is monitoring 279 pregnant women, including 122 in U.S. territories, the government agency reported at a news conference May 20.

Those numbers are way up compared with previous counts: Last week, the CDC tallied 47 cases in the states and 65 in the territories. The increase reflects a change in reporting, rather than a spike in new cases, said CDC epidemiologist Margaret Honein, who heads the agency’s birth defects branch.

Before today, the CDC report included only pregnant women who had both positive lab test results and either symptoms or pregnancy complications linked to Zika. The new tally includes women without symptoms of infection.

“We’ve learned a lot in the past four months,” Honein said. Scientists have reported that asymptomatic mothers have given birth to Zika-infected babies with microcephaly or other birth defects, she said.

So far, less than a dozen of the 279 U.S. pregnancies have had adverse outcomes, but the agency wouldn’t specify what those outcomes were, or how many women have given birth, miscarried or terminated their pregnancies.

In the United States, Honein said, microcephaly typically affects six per 10,000 infants.

Scientists have found one of the youngest exoplanets ever, huddling close to a star that is just 2 million years old. Located 450 light-years from Earth in the constellation Taurus, the star is so young that it still has its baby fat — it is surrounded by the disk of gas and dust from which it formed.

The planet, CI Tau b, is hefty for an infant — tipping the scales at 11 times the mass of Jupiter, say astronomer Christopher Johns-Krull of Rice University in Houston and colleagues in a paper posted May 25 on arXiv.org. It’s surprising, the researchers say, that such a large planet could have formed in just 2 million years — peanuts on cosmic timescales.
Such baby-faced exoplanets have been spotted before (SN: 12/26/15, p. 14), but they’ve lingered farther from their stars. This fledgling planet shows that such behemoths can form quickly and snuggle close to their stars. Scientists still don’t know whether star-hugging planets form far away and migrate inwards, or whether they are birthed close to their stars. The new planet could shed light on that process.

The scientists used a variety of optical and infrared telescopes to reveal periodic variations in the frequency of the star’s light, caused by the planet’s gravitational pull. CI Tau b tugs its star back and forth as it swings around in a tight orbit that it completes every nine days, the researchers determined. Hints of the planet showed up in both optical and infrared light, ruling out spurious signals caused by sunspots or other variability within the young and active star.

Editor’s note: Science News astronomy writer Christopher Crockett is a coauthor on the paper, which incorporates work he did as an astronomer at Lowell Observatory in Flagstaff, Ariz., prior to joining Science News.

Harnessing the weirdness of the quantum world is difficult — fragile quantum properties quickly degrade under typical conditions. But such fragility could help migrating birds find their way, scientists report in the June New Journal of Physics. Some scientists believe birds navigate with sensitive quantum-mechanical compasses, and the new study suggests that quantum fragility enhances birds’ sense of direction.

Molecules known as cryptochromes, found within avian retinas, may be behind birds’ uncanny navigational skills (SN Online: 1/7/11). When light hits cryptochromes, they undergo chemical reactions that may be influenced by the direction of Earth’s magnetic field, providing a signal of the bird’s orientation.
“At first sight, you wouldn’t expect any chemical reaction to be affected by a magnetic field as weak as the Earth’s,” says study coauthor Peter Hore, a chemist at the University of Oxford. Quantum properties can strengthen a cryptochrome’s magnetic sensitivity, but their effect sticks around only for tiny fractions of a second. Any chemical reactions that could signal the bird would have to happen fast enough to skirt this breakdown.

But Hore and colleagues’ new simulations of the inner workings of cryptochromes show that a little bit of quantum deterioration can actually enhance the strength of the magnetic field’s effect on the chemical reactions.

According to scientists’ theories, light striking a cryptochrome produces a pair of radicals — molecules with a lonely singleton electron. These unpartnered electrons feel the tug of magnetic fields, thanks to a quantum property known as spin, which makes them behave a bit like tiny bar magnets. But those minuscule magnets are not enough to serve as a compass on their own — instead, the electrons’ magnetic sensitivity is the result of a strange quantum dance.

The two radicals’ electrons can spin either in the same direction or opposite directions. But rather than choosing one of these two options, the electrons pick both at once — a condition known as a quantum superposition. Quantum mechanics can describe only the odds that the electrons would be found in each configuration if forced to choose. As time passes, these probabilities oscillate up and down in a pattern that is swayed by Earth’s magnetic field. These oscillations in turn affect the rate of further chemical reactions — the details of which are not well understood — which signal to the bird which direction it’s facing.

These chemical reactions must happen quickly. As the electrons interact with their environment, their coordinated oscillations dissipate, weakening their magnetic sensitivity. But Hore and colleagues show that this isn’t the complete picture — some loss of quantumness can help birds navigate. “Not only does it not hurt the compass signal, it can make it stronger,” says physicist Erik Gauger of Heriot-Watt University in Edinburgh, who was not involved with the research.
That’s because the direction of the magnetic field also determines how quickly electrons lose their coordination, further enhancing the difference in the chemical reaction rates based on the bird’s direction in the magnetic field. So the magnetic field does double duty: It affects chemical reaction rates by altering the oscillating states of the electrons and by determining when they break off their oscillation.

Although similar types of sensitivity-boosting effects have been suggested before, they weren’t based on a cryptochrome model, says Gauger.

It’s still not certain that birds navigate with cryptochromes at all, says Klaus Schulten, a computational biophysicist at the University of Illinois at Urbana-Champaign. More research is needed to understand the details of how the cryptochromes might function. “There, this paper is very valuable,” he says. “It’s an interesting idea that’s worth pursuing.”

“Junk DNA” may be an essential part of a worm’s inheritance.

Parts of this not-so-disposable DNA serves as a “watermark” to authenticate a Caenorhabditis elegans roundworm’s own genes and distinguish them from foreign genes that need to be shut down, researchers report in the July 14 Cell.

Genes bearing the watermarks — called PATCs — are protected against being shut down. These genes also tend to be active in the germ line (eggs and sperm and the cells that give rise to them). Genes without authentication codes get turned off, especially in the germ line, the researchers discovered. That raises the possibility that other species, perhaps even humans, issue their own germline gene work permits.
Researchers have known that C. elegans’ set of genetic instructions, its genome, is littered with PATCs (short for periodic An/Tn clusters), but didn’t know why. PATCs are short stretches of the DNA building blocks adenine or thymine separated by other building blocks, or bases; each run goes about 10 bases on average until the start of the next A or T cluster (for instance, TTTTTaatggAAAA etc.). About 10 percent of the worm’s genome is marked with the A or T clusters, says study coauthor Christian Frøkjær-Jensen, a geneticist at Stanford University.

While other animals don’t seem to have the regular patterns of A’s and T’s exactly like C. elegans does, “the general idea that species can mark segments of their genomes and protect them from silencing … could apply to other organisms,” says Andrew Spence, a geneticist at the University of Toronto who was not involved in the study.

In 2006, Stanford University geneticist Andrew Fire and colleagues pointed out that the A-T tattoos were often associated with genes that are active in the germ line. Those watermarks were found in filler DNA, called introns, sandwiched between the parts of a gene containing the information used to make protein. Introns are snipped out and thrown away before an RNA copy of a gene is read by protein-building machinery. Introns sometimes contain information about how to regulate genes. That seems to be what the PATCs are doing.

Fire and colleagues postulated that the PATCs helped C. elegans protect its own genes from being disabled by molecular defense mechanisms that halt the incursion of foreign DNA. (Fire won the 2006 Nobel Prize in physiology or medicine (SN: 10/7/06, p. 229) for the discovery of one such mechanism, a gene-silencing system called RNA interference or RNAi.) Alien DNA from viruses or selfish bits of genetic material known as transposons, or jumping genes, can wreak havoc on a genome, damaging genes that they hop into. It is important to stop the jumping genes in the germ line because DNA in those cells will be passed on to future generations.

To combat the jumpers, C. elegans and other organisms deploy an army of small interfering RNAs that shred RNA copies of foreign genes. Other small RNAs, known as piRNAs, direct cell machinery that stretches molecular hazard tape across DNA where transposons and other aliens settle. Such off-limits territory is called heterochromatin, and genes there are turned off. Sometimes, though, some important native genes that need to stay on get trapped behind the lines. PATCs may be the operating permits that let native genes in heterochromatin remain active.
In 2006, Fire and colleagues had no data to back up their idea. The new study puts Fire’s hypothesis to the test. “Oh my gosh, did they test it. It is really a thorough and complete analysis,” says geneticist Susan Strome of the University of California, Santa Cruz.

In the new study, Fire, Frøkjær-Jensen and colleagues engineered a gene for a fluorescent jellyfish protein with an intron containing PATC watermarks. When the researchers inserted the PATC-containing gene in a heterochromatin region of the genome, the gene turned on and made the worm’s germline cells glow. But the same jellyfish gene without PATCs was turned off. Those results are evidence that PATCs protect genes against getting turned off. Exactly how that happens isn’t yet known.

Strome isn’t sure that other organisms need DNA certificates to allow their genes to turn on in rough neighborhoods. C. elegans worms have unusual chromosomes. Nearly two-thirds of each chromosome is heterochromatin wasteland. The PATC permits may be necessary only in such extreme cases, she says.

Fire says he’s not yet ready to declare that all junk DNA may be useful. “Certainly there is gold in what we see here,” he says, “but the question is whether it is all gold.”

Before the demise of Japan’s latest X-ray satellite, Hitomi, the probe might have put to rest speculation about radiation from dark matter in a cache of galaxies.

In 2014 astronomers reported that several galaxy clusters appeared to inexplicably produce X-ray photons with energies of about 3.5 kiloelectron volts. The researchers suggested that the radiation could be coming from the decay of sterile neutrinos — hypothetical particles that are one candidate for the elusive dark matter that is thought to bind galaxies and clusters together.

Before the Hitomi X-ray satellite (aka ASTRO-H) failed on March 26, it got a look at the Perseus galaxy cluster, a horde of galaxies about 232 million light-years away. The telescope saw no sign of the previously reported X-ray photons, scientists report in a paper online July 25 at arXiv.org. A similar search of the dwarf galaxy Draco last year with the XMM-Newton satellite also failed to turn up the mystery X-rays. The no-show photons make it less likely that sterile neutrinos are the dark matter particles that scientists have been looking for.

Hitomi spun itself to death less than six weeks after it launched, when a problem with its control system caused the spacecraft to rotate out of control. The Japanese space agency is considering building Hitomi 2.0 for a possible launch in 2020.

The brains of human ancestors didn’t just grow bigger over evolutionary time. They also amped up their metabolism, demanding more energy for a given volume, a new study suggests.

Those increased energy demands might reflect changes in brain structure and organization as cognitive abilities increased, says physiologist Roger Seymour of the University of Adelaide in Australia, a coauthor of the report, published online August 31 in Royal Society Open Science.

Blood vessels passing through bones leave behind holes in skulls; bigger holes correspond to bigger blood vessels. And since larger vessels carry more blood, scientists can use hole size to estimate blood flow in extinct hominids’ brains. Blood flow in turn indicates how much energy the brain consumed. (In modern humans, the brain eats up 20 to 25 percent of the energy the body generates when at rest.)
Seymour and colleagues focused on the carotid arteries, the vessels that deliver the bulk of the brain’s blood. The team looked at nearly three dozen skulls from 12 hominid species from the last 3 million years, including Australopithecus africanus, Homo neanderthalensis and Homo erectus. In each, the researchers compared the brain’s overall volume with the diameter of the carotid artery’s tiny entrance hole at the base of the skull.
“We expected to find that the rate of blood flow was proportional to the brain size,” Seymour says. “But we found that wasn’t the case.” Instead, bigger brains required more blood flow per unit volume than smaller brains.
The boost in blood flow, and therefore metabolism, suggests two possible conclusions, Seymour says. As hominid brains got bigger, they might have packed in more nerve cells, or their nerve cells might have fired more frequently. Either way, he argues, the increased blood flow suggests greater brainpower, perhaps reflecting reorganization of the brain over the course of evolution.

But not all of the blood coming into the brain through the carotid arteries directly supports mental prowess. “You need more complicated wiring for bigger and more cognitively advanced brains,” says Dean Falk, an evolutionary anthropologist at Florida State University in Tallahassee. “But those brains have more advanced cooling requirements.”

Some of the blood coming in through the carotid arteries absorbs heat generated by the brain’s activity and then drains away, helping to keep the brain cool, Falk says. So while the study is a scientifically rigorous look at metabolism and blood flow toward the brain, she says, a follow-up study is needed to account for the blood moving away from the brain.

Lawrence David’s gut check gets personalA Jim Carrey movie inspired computational biologist Lawrence David to change the course of his research. As a graduate student, David saw Yes Man, a 2008 film in which Carrey’s character is forced to say yes to all propositions.

David thought the movie’s message about opening yourself to new experiences, even uncomfortable ones, might make science more exciting than it already was. “Only good things would happen if I loosened up and said yes to everything,” he says.

The next day, his graduate mentor at MIT, Eric Alm, was talking about the brand-new science of the human microbiome, the collection of bacteria, viruses and other microscopic organisms inhabiting the human body. What someone ought to do, Alm suggested, is sample a person’s feces every day for a year to see whether the microbiome changes. “I had just seen the movie, so I said, ‘Well, I guess I have to say yes now,’ ” David recalls.
David took Alm’s suggestion a step further by chronicling his own microbiome, collecting his feces every day in “plastic hats that look like something the Flying Nun would wear.” He washed his mouth with a chemical solution and spit into a tube to harvest mouth bacteria, popping all the samples into his refrigerator or freezer until he could get them to the lab. He customized an iPhone diary app so he and Alm, who joined the study, could track 349 different health and lifestyle measures, which included the timing and consistency of bowel movements, sleep quality and duration, blood pressure, weight, vitamin use and mood. They noted, in detail, the foods they ate, symptoms of any illnesses and medications used to treat those illnesses. By the end of the year, David had “10,000 measurements of how two people lived their lives.”
David, now 33 and at Duke University, regularly opens himself to new scientific challenges, though they aren’t always quite so personal. Before finishing his degree at MIT, he had already initiated one new field of research and delved into several others outside his expertise.

Awards committees and granting organizations have taken note. David has won the Beckman Young Investigator award and the Searle Scholars award, which support cutting-edge work by young scientists. Fresh out of graduate school, he became a junior fellow at Harvard, where he led his own research.

“He has an ability to see what the problem is and just get it done in the most straightforward way possible,” Alm says.
David spent most of his graduate student years in Alm’s lab writing and running computer code that calculated the ancient birth dates of genes, reproducing the most likely evolutionary histories of gene families and predicting capabilities of ancient microbes. Alone that would have been a nice contribution; many researchers thought untangling those relationships would be too computationally complex, Alm says.

But to get the full picture, David had to expand into other fields, working with geologists and geochemists to determine whether his predictions made sense in light of Earth’s geologic history. In a study that birthed a new field by marrying geochemistry and genetics, he and colleagues discovered that genes encoding oxygen-producing proteins appeared hundreds of thousands of years before oxygen began accumulating in early Earth’s atmosphere (SN Online: 12/21/10). For a study published in Science in 2008, he also delved into ecology, investigating how ocean microbes evolve into separate species without the physical boundaries that would keep them from mixing.

Population flux
The personal microbiome challenge was an unprecedented look at how friendly bacteria change over time and with lifestyle and dietary choices. Long known to play an important role in digestion, the gut microbiome has recently been implicated in health conditions including heart disease, obesity and asthma, and may even influence behavior (SN: 4/2/16, p. 23). Many people have suggested that humans and their microbes are so interdependent, they should be considered composite organisms (SN: 1/11/14, p. 14).

David, Alm and colleagues presented the results of their study in 2014 in Genome Biology. They found that the gut microbiome remains stable for months, but some events, such as travel, illness or changing the fiber content of the diet, can rapidly change the mix of gut microbes. Only a handful of studies have ever been done on this fine of a timescale, Alm says.

A project that would have made others hold their noses “might have been the most enjoyable thing I’ve done in science,” David says. The microbiome analysis relied on computer tools similar to ones he had used as an undergraduate researcher at Columbia University, making it intellectually satisfying.

But the real appeal was how others responded to the work. “People were immediately captivated by the work, and would start to tell me about their own gastrointestinal histories, odd things they had eaten and how that affected the bacteria in their gut,” David says. People sometimes asked his advice on what to eat to keep their gut microbiomes healthy, a question for which he didn’t have a clear answer. “There’s an irony to this,” he says. His voice drops to a whisper as he confesses: “I love junk food…. I shouldn’t be a poster child.”

Hooked on the microbiome, David began studying other people’s bacteria with the help of Peter Turnbaugh, a microbiologist then at Harvard and now at the University of California, San Francisco. By intentionally manipulating people’s diets, the researchers found that it takes only a day for a major dietary change, such as a meat-eater going vegetarian, to shift the composition of gut bacteria. The results, which surprised researchers who had thought such shifts would be more gradual, were reported in Nature in 2013 (SN Online: 12/11/13).

When he arrived at Duke in 2013 to start his own lab, David had a strong track record of developing computational tools to analyze complex datasets, says John Rawls, a microbiome researcher at Duke. But what makes David special isn’t just that he’s a good computer coder. “What sets him apart is his ability to incorporate technology and concepts from engineering into his work,” Rawls says.

Most labs that study the microbiome start with animal studies. But David began with a machine — an artificial gut for growing and manipulating intestinal microbes donated by human volunteers. The contraption consists of multiple growth chambers bristling with plastic tubes. Inside, what David has called “the world’s nastiest slurry” (a fecal sample from a donor) ferments in conditions similar to those in the intestines. One tube feeds into what looks like a dome hair dryer from a beauty salon. That’s a concession to neighboring researchers who complained about the pungent smell.

When graduate student Rachael Bloom joined the lab, David persuaded her to try a completely different way of growing bacteria from feces, designing chips with channels that separate out bacteria into microscopic drops of liquid. In just a few minutes, Bloom can create what are essentially thousands of tiny petri dishes, each with a single bacterium. Neither student nor mentor had any experience with the “microfluidics” technique, but David encouraged Bloom to try, and even be open to failure. “In retrospect, that could be really dangerous,” says Bloom, “but I have learned so much.”

David’s aptitude for engineering shows up at home, too. To keep his two preschool children from getting up too early, David rigged LED lights on a timer. The kids have to wait for the lights to go off before getting out of bed. His wife, a psychiatrist, reinforces the good behavior with a treat.

David says he “tends to be an optimist,” and just assumes his team will find a way over or around any hurdle. “He’s very adventurous. He’s very creative,” says Turnbaugh. “He’s one of the great people in microbiome research who is thinking outside the box and not just following a template.”

David has a simple explanation for why he continues to say yes to projects outside his comfort zone: “I’m easily fascinated.”