The husband and wife researchers are just starting their own prion experiments at the Broad Institute lab where they work. 
 
 Sonia Vallabh and her husband, Eric Minikel, walked into an examining room at Brigham and Women’s Hospital on an unusually warm December morning in 2011, two months of waiting down to final minutes. She was about to learn if she carried a genetic mutation for a rare disease that kills sufferers by stealing their sleep, their memory, and, eventually, their consciousness. The illness, fatal familial insomnia, or FFI, usually strikes at about age 50. Sonia was 27. 
 
 Sonia and Eric sat down. Two women, hospital employees, chatted and laughed as they moved around the room. Is this a sign? Sonia wondered. If we’re about to receive life-changingly bad news, surely no one would be laughing, right? 
 
 Then the doctor, carrying a paper with her test results, and a genetic counselor walked in. “The same change that was found in your mother was found in you,” the doctor told Sonia. Medicine had no treatment or cure for the disease, he said, but researchers had made important advances. He and the counselor left, giving the couple privacy to talk. Eric dove toward Sonia, throwing his arms around her. As terrified as they felt, it was better to know. 
 
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 Earlier in the fall, they’d flown to Sonia’s hometown in western Pennsylvania for a friend’s engagement party. Sonia’s father took her aside just before they left. “It’s about Mom,” he said, and her heart sank. Her mother had died a torturous death the previous year, less than 12 months after she had first turned forgetful. Soon she couldn’t finish sentences. She hadn’t slept, night after night, and had sunk quickly into dementia. She died at 52, two days before Christmas in 2010. Doctors hadn’t been able to diagnose her illness. Now Sonia’s father told her the autopsy had discovered she had FFI, a rare, genetic form of prion disease. Sonia had a 50 percent chance of inheriting the gene. 
 
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 Sonia kept quiet on the ride to the airport with Eric and as they passed through the labyrinth of security at Pittsburgh’s airport and boarded the plane home to Boston. After they’d buckled into their seats, she finally told him what her father had said. Eric clung to her, feeling as if he couldn’t breathe. 
 
 Not long after, Sonia had her blood drawn for the test. Then they waited. They flew to Japan for a delayed honeymoon. They tried to distract themselves with work. Sonia had recently graduated from Harvard Law School and had a job as a consultant, Eric as a transportation technology consultant. And they began to study prions, the mysterious proteins that were the source of the disease and whose purpose no one yet understands. 
 
 Friends and relatives had raised the possibility of not testing Sonia for the mutation. There is no treatment or cure for FFI; did the couple need to live under that shadow? But Sonia and Eric agreed — they had to know. They were already filled with dread. If the test were positive, it would confirm fears that already existed: that, like her mother, Sonia could remain healthy until suddenly, at around age 50, she wouldn’t be able to sleep much. She would labor to walk. She would lose her mind and likely die within a year. 
 
 But that same night after learning her test results, Sonia devised a coping mechanism, a way of thinking about the disease that calmed her and carried her through the early weeks. “Here is this day in my life,” she told herself. “Neither today nor tomorrow nor for the next week is it likely that this will happen to me.” The next day, she told herself the same thing. 
 
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 Her body had not changed. Since the moment she was conceived, a tiny error had been embedded in one of her two copies of chromosome 20, the copy inherited from her mother. The only difference: Now she knew. That knowledge would transform — and, in some ways, dismantle — the life she and Eric had begun together. But not in the ways she expected. 
 
 THE TWO WERE IN THEIR 20s when they met in Northern California, where each had moved after college. Eric, who lived in Oakland, had been invited to a dinner party in Berkeley hosted by Sonia’s housemate. Sonia had gone out that night but came home during the party. When she smiled at the table of guests, Eric saw a warmth that suggested curiosity, optimism, a willingness to be surprised and delighted by life. He thought I’ve got to get to know her. 
 
 They talked, and the next day they hiked through the rain, across hills and valleys where mercury had once been mined. The hike turned into dinner, then a friend’s party, and a 2 a.m. goodbye. They fell into an intense friendship; after three months, they started dating. Soon Eric confessed he loved her. 
 
 Their families and friends began to suspect the pair were serious. “They have a unique passion for each other that I think is not very common among couples,” says Michelle Minikel, Eric’s sister. She noticed a change in her brother: “He just got much happier when they got together.” 
 
 Eric and Sonia applied to graduate schools — law for Sonia and city planning for Eric — and agreed to study in the same city. After they got accepted to schools in Philadelphia, they spent a day touring campuses. That night, stretched out on the sofa bed of a friend of a friend, they talked, acknowledging for the first time that their plan might not work. Eric had also been accepted at MIT, and he really wanted to go, but Sonia hadn’t heard yet from her Boston school, Harvard Law. What would happen to their relationship if they lived apart? 
 
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 “I was just saying, in the aggregate, long distance is hard on people,” Sonia says. “Assuming we fall into that general population, it’s likely to be hard on us.” 
 
 “That’s when I realized I had to lock it down,” Eric says. “So I asked her to marry me.” 
 
 When Sonia got accepted to Harvard Law, they moved to Cambridge and Eric began the MIT program. They married after their first year of grad school, in the summer of 2009, in Sonia’s parents’ backyard in Pennsylvania. Each took the other’s last name as a middle name. Sonia’s mother planned the wedding. 
 
 After Sonia’s diagnosis in late 2011, life changed. They threw themselves into learning everything they could about prions and fatal familial insomnia. Neither had studied much science post-high school, so they held a weekly “science night” at their apartment near Central Square with friends who taught them the basics of biology and chemistry. They took classes at Harvard Extension School. And they created the Prion Alliance, a nonprofit devoted to research into the treatment or cure of prion disease. 
 
 Shortly after her diagnosis, Sonia left her consulting job to study science full time. She also started work as a stem cell technician at Massachusetts General Hospital’s Center for Human Genetic Research. Then Eric quit his transportation job to work in the same MGH department, writing code to analyze DNA and RNA sequences. The first two years were exhausting. And the science they were learning on the job did not teach them about FFI. So they studied prions at night and on weekends. Eric saved scientific papers on his phone, opening them on the Red Line between home and work, or at night when he couldn’t sleep. 
 
 Dina Rudick/Globe staff Sonia Vallabh and her husband, Eric Minikel, are in a race against the genetic mutation she inherited from her mother that will cause fatal familial insomnia. 
 
 Through their tiredness, they learned a new way to be a couple. “It’s amazing to already be in love with someone and see them grow and impress you in new ways that you never imagined,” Eric says. His computer background now helps them analyze data, and Sonia’s work in molecular biology helps them as they begin their own research. They have found they learn faster if they work together. 
 
 Sonia is quieter and more pragmatic, patient where he moves ahead quickly. She tells the story of how they met in chronological and geographical order. Eric turns to her and says with a smile: “You’re leaving out all the rich emotional detail.” 
 
 A TURNING POINT IN THEIR CAREERS CAME in May 2014, when they flew to Trieste, Italy, for the annual international meeting on prion disease research. The scientific poster they presented, summarizing their early research examining whether all prion protein mutations caused disease, won a prize in the human disease category. When the winners were announced, Eric teared up. “Early on, I worried people wouldn’t take us seriously,” he says. “That we’d always be sort of a curiosity or sideshow.” 
 
 So many people came up to them to ask about their research that they didn’t even have time to claim their 300 euro prize. It came months later, after they were back home in Cambridge. 
 
 Byron Caughey is a senior investigator at the Rocky Mountain Laboratories in Hamilton, Montana, a facility run by the National Institutes of Health. Caughey, who was in Italy to see Sonia and Eric win the poster prize at Prion 2014, has been in contact with them for several years. The lab has been studying prion disease for decades, and the couple have traveled to the lab several times. Caughey helped them learn the basics of prion lab research. “It’s a testament to their raw talents,” he says. “It really is extremely difficult for people to come in from the outside and so rapidly gain the background and the sophistication and even the language that’s required to be effective in scientific research. . . . Now they’re a strong presence in the field.” 
 
 Both Eric and Sonia were admitted to a PhD program in biological and biomedical sciences, starting at Harvard Medical School in fall 2014. And last May, Stuart Schreiber, one of the founders of the Broad Institute of MIT and Harvard, invited them to join his lab, which researches small-molecule therapeutics. 
 
 Schreiber agreed to work with them even though he knew little about prion disease. “When a force of nature meets a force of nature meets a tragedy, what do you get?” Schreiber asks. “You get Eric and Sonia. They have a voraciousness for information. They have an otherworldly intellect.” 
 
 They spend much of their day sitting side by side at their desks, elbows almost touching. “We were never much into personal space,” Eric says. 
 
 Other patients have raised money and started companies to cure diseases that have targeted them or their families. But no one seems to have gone as far as Sonia, now 31, and Eric, 32. They’ve given up their intended careers to become scientists, devoting their lives to curing her disease. 
 
 “Eric and Sonia are unique in the directness of their engagement,” Schreiber says. 
 
 When the couple began to think about switching careers to research scientists, they often talked to his sister, Michelle, a doctor in Green Bay, Wisconsin. She warned them that developing a single drug can take a decade or more. “Research is slow and agonizing and tedious,” she says. She also knew how much Eric loved his job in transportation planning and worried he would miss the work. But after they made the change, she saw Eric and Sonia’s commitment to prion research and realized its worth to them. 
 
 “No matter what we were doing, you could tell they were constantly thinking about it,” she says. 
 
 Michelle had seen her brother’s intense drive during the year they lived together at the University of Wisconsin-Madison. He had planned to major in computer science but switched to Chinese. She watched him practice Mandarin for hours, repeating words over and over, to perfect his pronunciation. 
 
 After graduation, when they were both living in California and Eric was tutoring immigrant children, he calculated that he would be able talk with about 80 percent of his students if he could improve his Spanish and pick up Arabic. She saw him devote himself, once again, to becoming fluent in new languages. 
 
 “Within a couple of years,” Michelle says, “he could walk up to someone and strike up a conversation in one of four languages.” 
 
 PRIONS ARE MYSTERIOUS PROTEINS whose very existence as agents of disease was once debated by scientists. Everyone has trillions of prion proteins on the surface of their cells, but researchers still don’t know what they contribute to our bodies. Prion proteins, like all proteins, are chains of amino acids. The order of amino acids in a protein causes regions of the protein to assemble — or fold — into specific shapes. Prion proteins can misfold into a different, disruptive shape. If a single prion protein misfolds, it can lead the other prion proteins to misfold and clump together. Clumps of prion protein, toxic to neurons, eventually kill them. 
 
 Stanley Prusiner, a neurologist at the University of California, San Francisco, who named the prion, had won the Nobel Prize in Medicine in 1997 for his research showing that prions cause degenerative brain diseases, such as Creutzfeldt-Jakob disease and bovine spongiform encephalopathy, or mad cow disease. All prion diseases are fatal. 
 
 For most of us, the chance of a prion protein randomly misfolding and causing one of these diseases is very low: Sonia and Eric estimate the odds are 1 in 5,000 or 10,000. But Sonia’s genetic mutation specifically instructs the prion protein to misfold. Research suggests that nearly everyone with her specific mutation — known as D178N (cis-129M), for the amino acids that are erroneously replaced — gets FFI, usually when they are about 50 years old. 
 
 Sonia’s mother was 51 when her health problems began to show up. She lost weight. Her eyesight diminished. She had a minor car accident, seemingly caused by an error in judgment. Two months later, she struggled to finish a sentence. “From there, things progressed very, very rapidly,” Sonia says. “So she went into progressive dementia, and once that happens, you just lose abilities one by one.” 
 
 Eric and Sonia know the power of their own narrative when they give talks at academic conferences. “We always lead with our story, and I think that inspires a lot of people,” Eric says. “I think people who are in academia for a long time are excited to meet people who are in it for something other than academic success.” He adds, “We’re lucky that it’s kind of an interesting disease.” 
 
 On January 20, Eric and Sonia published their first joint paper. They worked with 23andMe, a consumer genetics company based in Mountain View, California, analyzing data from 530,000 of its customers and from thousands of prion disease cases and other samples. (Most of the people who pay 23andMe for a DNA analysis have agreed to volunteer their data for research.) When Eric and Sonia analyzed the data for the 63 known genetic mutations believed to cause prion disease, they found that almost 1 in 1,000 people had one of those mutations. But only about 1 in 50,000 dies from genetic prion disease. (About 1 in 5,000 dies from prion diseases, but most of those cases occur spontaneously, rather than being handed down genetically.) 
 
 Not all of the genetic mutations cause disease, they concluded. Unfortunately, as they had suspected, Sonia’s mutation was not one of the benign mutations. Others, though, have already benefited from their findings. Their research led Dr. Robert C. Green, a medical geneticist at Brigham and Women’s Hospital, to tell a patient her mutation, previously thought to be fatal, was probably harmless. 
 
 The paper also offered tantalizing hope for future treatment for prion disease. Eric and Sonia found three people with another kind of mutation — one that gave them only one working copy, rather than the normal two — of their prion protein gene. These three people, including a 78-year-old woman, seemed to be generally healthy. 
 
 “This is an important discovery by Eric and Sonia that opens up a new and promising direction for discovering a drug to treat the prion disease,” Stuart Schreiber says. 
 
 The couple are buoyed by this hope — the potential creation of a “gene-silencing” drug to turn off the mutated copy of the prion protein gene — even though they know it faces many hurdles. They received a $40,000 BroadIgnite grant, designated for young scientists with creative ideas, to outfit their lab and start research. They’re just beginning their own experiments, developing a human cell model of prion disease using a new method to track prions and studying healthy prion protein in hopes of discovering ways to treat prion disease. 
 
 And they have a life ahead of them, even if it’s not the life they once imagined together. Sonia finds far more meaning in her work than she ever found in the law. Someday, she and Eric would like to have children who don’t carry the genetic mutation. They hope to conceive through in vitro fertilization, using a procedure that has emerged for couples that don’t want to pass on genetic diseases to their children. Embryonic cells would be tested for the genetic mutation and only embryos with no detected mutation would be transferred to Sonia’s uterus. 
 
 Last fall, Sonia and Eric spoke at the Broad to a room full of donors. Eric told them he and Sonia initially thought they had suffered terrible luck, but then they realized they had been given a chance. “It’s an incredibly special thing to have 20 years’ advance notice to work like hell to change the fate that you’ve been given,” Eric says. 
 
 He remembers his first glimpse of Sonia and how her smile drew him to her, full of curiosity, full of promise. “Maybe it’s a lot to read into a smile,” he wrote recently. “But the years have shown that I wasn’t wrong. I think fundamentally she believes . . . that the world is an incredible place, a place that can surprise you and where you can surprise yourself. And somehow, believing it makes it true, because that’s how her life has been, and since we got together, that’s how my life has been too.” 
 
 This story has been updated to clarify who attended the Broad Institute presentation last fall. 
 
 Kathleen Burge, a writer in Belmont, is a former Boston Globe reporter. Send comments to magazine@globe.com ||||| When young love faces death, tragedy too often follows. But what if science throws in on the side of the lovers? 
 
 Husband and wife Eric Minikel and Sonia Vallabh, both Harvard Ph.D. students, have through fate and choice become a test case. The couple has embarked on a journey both personal and scientific, one that began five years ago in a mother’s horrifying decline into dementia and death from a rare brain disease, the tracks of which appear in Vallabh’s DNA. 
 
 Their search for a treatment is off to an encouraging start. Still relative newcomers to the lab, Vallabh and her husband have two research papers under their belts, and have exhibited enough energy and intellect to make some of the world’s top scientists enthusiastic supporters and cautious believers. The genetic bomb of prion disease that killed Vallabh’s mother is almost always fatal, but usually doesn’t strike until middle age, still years away for her 31-year-old daughter. In the meantime, every moment counts. 
 
 “When a force of nature meets a force of nature meets a tragedy, what do you get? You get Sonia and Eric,” said Stuart Schreiber, the Morris Loeb Professor of Chemistry and Chemical Biology and the head of the Broad Institute lab where Vallabh and Minikel are conducting research. “I don’t know the final outcome, but I think the early steps toward remedy look promising. They bring otherworldly intellect with a heavy dose of urgency to prion disease.” 
 
 A devastating decline 
 
 It’s a long way to brain science from transportation planning, in which Minikel trained at MIT, and alternate dispute resolution, which was Vallabh’s focus after graduating from Harvard Law School in 2011. 
 
 The journey began in early 2010. The couple, living in the 630-square-foot Central Square apartment they’d shared since moving to Cambridge from California in 2008, started to hear from Vallabh’s mother, Kamni, that she was losing weight and having trouble with her vision. 
 
 “It just seemed like minor things,” Vallabh said. “Winter in western Pennsylvania can be a tough time for everyone. I was thinking, ‘It’s not a great winter for Mom.’” 
 
 But when Vallabh visited home in May, her mother’s deterioration was frightening. 
 
 “It happened really quickly that she wasn’t able to get to the end of a sentence without losing her train of thought, trailing off into murmuring or into non-sequiturs,” Vallabh said. Her mother “couldn’t remember for any period of time that she wasn’t strong enough to stand or walk. If you turned your back for a second, she would try to stand and fall.” 
 
 The family’s search for answers took them to specialists in Pittsburgh, Cleveland, and Boston, but the doctors were stumped. Lyme disease and heavy-metal poisoning were among the possibilities considered and then dismissed. An early spinal tap to check for prion disease came back negative. 
 
 “Every time there was a new hypothesis … there was an uptick in hope for the whole family,” Vallabh said. “Then it would fade away.” 
 
 Kamni’s condition worsened. In and out of hospitals, she underwent a tracheotomy and was put on a respirator. She developed pneumonia and, finally, in December, after nearly a year of rapid decline, underwent another spinal tap. It came back positive: a tentative diagnosis of sporadic prion disease. 
 
 Vallabh’s mother died on Dec. 23, 2010, still lacking a confirmed diagnosis. Her father, Sagar, decided to have an autopsy done, but the results would take some time. Vallabh returned to Cambridge to finish her legal studies, graduating from Harvard Law in May and starting work at a small consulting firm in Boston. 
 
 A few months later she was back in Pennsylvania for a friend’s engagement party. At the airport for her return flight, her father asked if he could talk to her alone. Kamni had indeed died from prion disease, he told her. And, though most cases develop spontaneously, her mother’s was genetic. 
 
 Lethal proteins 
 
 It took science some time to come around to the idea that disease might spring from proteins, which seemed strange bedfellows with viruses and bacteria. Proteins are important elements in the diet and essential to the body, providing the building blocks for muscle, red blood cells, hormones, enzymes, and a wide array of other tissues. 
 
 But they can go wrong. Proteins are long molecules, containing hundreds or even thousands of atoms that fold themselves into 3-D structures. These structures are characteristic for each protein and influence how they work. Folds can expose or hide parts of a molecule, making them more or less likely to interact. In prion disease, prion proteins begin misfolding into a malignant form. 
 
 The genetic mutations that can cause genetic prion disease all occur in the prion gene, PRNP, and are dominant. That means that only one copy is needed to seed disease and that Vallabh had a 50 percent chance of inheriting the copy from her mother. 
 
 Though several different prion-related diseases are recognized by medical science, Minikel and Vallabh have come to believe that they’re all variants of the same condition, traced to different mutations of PRNP and the misfolded protein it encodes. 
 
 On the flight back to Boston, Vallabh told her husband the news. 
 
 “I couldn’t get enough air in my lungs to breathe,” Minikel said. “I was holding Sonia … not letting go. The flight attendant kept coming by — ‘Are you OK?’ We weren’t, but what could we say?” 
 
 With no treatment or cure, someone else might have passed on testing for the gene. 
 
 But Vallabh’s decision was immediate: She had to know. 
 
 “We can never go back to a time [when] we didn’t have the question,” Vallabh said. “Rather than live with the question, I wanted to have the answer.” 
 
 In December 2011, several torturous weeks after providing a sample, Vallabh met Minikel amid the bustle of Park Street station. They rode the E train out to Brigham Circle and walked a short distance to Brigham and Women’s Hospital. 
 
 When the geneticist and a genetic counselor came in, they delivered the news simply: “The same change that was found in your mother was found in you.” 
 
 As the information sank in, Vallabh heard the geneticist say that he was “cautiously optimistic” a treatment would be developed eventually. But in the moment, there was no escaping the likelihood that her mother’s fate would be her own. 
 
 After the couple shared the test results, friends converged on the Central Square apartment, and Vallabh’s father flew to Boston. The weekend passed in a sort of mourning, as the couple and those closest to them absorbed the news and tried to understand what it meant for the future. 
 
 “That grieving process lasted a week,” Vallabh said. “Then we had a visit from Stevie.” 
 
 Help from a friend 
 
 Stevie Steiner was a doctoral student at MIT and an old friend of Minikel’s. The two had met in 2000 as freshmen at the University of Wisconsin at Madison, bonding as fellow nerds. They lost touch after graduation, but reconnected in Cambridge thanks to a chance meeting on a corner near the MIT campus. 
 
 When Steiner heard about Vallabh’s diagnosis, he was unconvinced. As a scientist, he held faith in the power of science, but he also remained clear-eyed on its limits, not least when it came to rare conditions such as genetic prion disease. 
 
 “My first reaction was, ‘We don’t know what we don’t know,’” Steiner said. 
 
 Steiner, working on his doctorate in materials chemistry and engineering, was no expert on the disease. But he knew that there was a lot more going on in prion labs than physicians would discuss with patients. He also knew that much of that work was available in scientific journals. So he searched for articles in a database, and then loaded them onto a flash drive. 
 
 Steiner “brought with him a very different energy,” Vallabh said. “Everyone [else] was, ‘Wow, this is hard.’ Stevie came in the door with his own agenda. 
 
 “He said, ‘Guys, science has answers. Don’t lie down and take it. Things are happening.’ This was so different, we almost couldn’t handle it.” 
 
 Steiner left the flash drive, but neither Vallabh nor Minikel touched it for several days. 
 
 “Some of my reluctance was disbelief,” Vallabh said. “My mother saw some of the best neurologists in the country and still died without a diagnosis. These diseases were too rare. It didn’t seem plausible to me that people were working on them.” 
 
 Finally, they plugged in the drive. 
 
 “What I didn’t appreciate was the [divide] between research and the clinical side. Looking at the articles I realized that maybe there’s nothing making it from the lab to the clinic now, but there’s a huge backstage warren of activity pointing in that direction. As soon as we realized that people are out there devoting their careers to working on prions, defining prions, understanding disease, and thinking about treatment, we started looking ourselves.” 
 
 The couple set off on their own search of journals, a search that soon became addictive for Vallabh. “It had an optimistic energy to it that I liked. It was helping, it [made] me feel better. It felt like a sabbatical from my normal life to get up to speed on science.” 
 
 In January 2012, she quit her job. 
 
 Lab lessons 
 
 Before long Vallabh was sitting in on MIT classes. Next she enrolled in a molecular biology course at Harvard Extension School. One night after class, she approached teaching assistant James Walker, a Massachusetts General Hospital (MGH) scientist and an instructor in neurology at Harvard Medical School (HMS). 
 
 “She told me the story from the beginning,” Walker said. “It was captivating. She was hesitant to say ‘This is what I want to do,’ but she was wondering whether there were opportunities.” 
 
 Vallabh asked Walker about possible volunteer positions in a lab. Though Walker knew Vallabh was a newcomer to science, he also knew she was smart and driven. He’d see what he could find. 
 
 It didn’t take long. Marcy MacDonald, an HMS professor of neurology and a Huntington’s disease researcher at MGH’s Center for Human Genetic Research, had an opening for a technician and agreed to take on Vallabh. The first day in the lab was surreal. 
 
 “I kept thinking, ‘Any minute now, I’m going to say something dumb and they’re going to take [this] away from me,’” Vallabh said. “It was very hard for me to accept that they hired me on the premise that I was a beginner and I’m really going to try hard.” 
 
 Vallabh survived the day, and over the weeks to come, won the respect of her lab mates. Marta Biagioli, then a third-year postdoctoral fellow, said she didn’t know what to make of Vallabh when she arrived. MacDonald had warned her that Vallabh was a beginner, so on that first day, Biagioli lined up a few simple tasks to ease her into her duties: use a pipette, make a solution. 
 
 The newbie proved a fast learner. 
 
 “She practically jumped from very basic pipetting to more complicated experiments in a couple of months,” Biagioli said. “That was really impressive to me.” 
 
 Vallabh soon realized her “sabbatical” from legal work was morphing into something more permanent. Her time in the lab felt meaningful beyond anything she could imagine in law. She and Minikel began to think about what came next. 
 
 ‘Engaging with science … is really different from thinking about my own mortality every day. In some ways one has displaced the other.’ —Sonia Vallabh 
 
 The couple had already founded the Prion Alliance, aimed at supporting work toward a treatment. Minikel began to blog about the disease and eventually followed Vallabh to MGH, leveraging his analytic skills and experience in an Extension School bioinformatics course to find work in a different lab. Formal scientific training emerged as the next shared goal. 
 
 At first the couple looked at schools where prions were a major focus, which left out Harvard’s Division of Medical Sciences, the Harvard Medical School-administered Ph.D. program of Harvard’s Graduate School of Arts and Sciences. Among the top candidate schools was the University of California at San Francisco, the base of Stanley Prusiner, who won a Nobel Prize in 1997 for his discovery of prions as a new kind of infectious agent. 
 
 Then, at a reception for prospective graduate students, Vallabh and Minikel struck up a conversation with Harvard’s Schreiber. He challenged the notion that the only path was an established prion laboratory. 
 
 An alternative, he offered, would be to join a multidisciplinary team of scientists who might not be expert in prions, but who knew a lot about modern therapeutics. He knew exactly where to look — his own lab. The plan held risks, not least that the prion expertise would depend on a pair whose primary training was in transportation planning and law. But the combination of therapeutics and prion research might just accelerate a treatment. 
 
 In the fall of 2014, Vallabh and Minikel entered Harvard’s biological and biomedical sciences Ph.D. program. And when it was time to find a lab for their research, they turned to Schreiber. 
 
 Onward, together 
 
 In January, Minikel and Vallabh were the first authors on a study with a fraught question at its heart: If you have the gene, what are your chances of getting the disease? 
 
 Some genes confer near-certainty that disease will develop, but most of the time cause is blurred, a blend of genetic roots — often from multiple genes — with environment and lifestyle. Minikel and Vallabh’s study used multiple databases of both sick and healthy people to investigate 63 different prion disease mutations, including the one Vallabh carries. 
 
 They were able to draw conclusions for 10, finding that three mutations thought to cause disease were likely benign and that three more caused disease in far fewer cases than originally thought. For four mutations, however, including Vallabh’s, they found “penetrance” to be nearly 100 percent. In other words, those who have the mutation will almost certainly develop the disease. 
 
 But the study also carried good news. It documented three people in good health even though one of their prion genes was shut off. Such a “loss of function” mutation means that drugs that might one day reduce prion protein in the body will likely be safe. 
 
 The research also eased the mind of at least one worried woman, according to Robert Green, a geneticist at Harvard-affiliated Brigham and Women’s Hospital. The daughter of a deceased patient who tested positive for prion disease had been concerned that the disease was genetic and that she herself was at risk. Minikel and Vallabh’s study showed that although the mother did have a mutation for prion disease, that particular mutation was likely benign, allowing Green to call and ease the daughter’s concerns. 
 
 For Schreiber, the article carried another benefit: It provided evidence of the couple’s scientific chops. The publication, their second, struck him as a sign of more to come. “Any one of these would be the paper of a lifetime,” he said, adding: “We believe in Sonia and Eric. I’m in it for the long haul.” 
 
 It’s a belief Minikel and Vallabh have taken to heart, making a second home of the Broad, which has provided separate lab space for their research and extra backing in the form of a BroadIgnite grant. 
 
 The couple once imagined speeding through doctoral studies to focus on prions in their own lab, but no longer. They have been able to dive right into prion research and draw on the material and intellectual resources — including platforms in genomics, metabolomics, proteomics, and small-molecule screening — of one of the world’s top biomedical research centers. 
 
 “I feel like we’ve landed,” Vallabh said. “We found our place where we can do science. We just got to do it, make the most of the opportunities here.” 
 
 Those opportunities leave scarce time to dwell on disease and the uncertainties of tomorrow. 
 
 “Engaging with science … is really different from thinking about my own mortality every day,” Vallabh said. “In some ways one has displaced the other. 
 
 “We’re optimistic and hopeful that we’re moving the ball forward. We can put energy there instead of spinning wheels for things I can’t affect.” 
 
 Meanwhile, the idea of raising a family is more and more on their minds. Vallabh and Minikel have fertilized embryos — safely frozen for now — that tests have shown are free of the genetic mutation for prion disease. Sometime in the next couple of years, they may take yet another leap. 
 
 “Some people have five or six generations of disease in their family,” Vallabh said. “To take it into our own hands to end transmission through your germline I think is miraculous. It’s so powerful. What an amazing gift to be able to give your kids.”
– In 2010, Sonia Vallabh noticed her mother acting oddly. "She was fitful and couldn't really tell you if she'd been awake or asleep," Vallabh tells CNN. Soon, the 52-year-old couldn't recognize her daughter and would spasm and speak in tongues. Upon her death months later, Vallabh recalls her father, a doctor, warning, "Her disease was genetic." Those words would change the course of Vallabh's life. Vallabh and her husband both quit their jobs and are now getting their PhDs in biology at Harvard Medical School in the hope that they can find a cure for fatal familial insomnia before it takes her life. FFI is caused by a gene mutation that Vallabh has inherited as a member of one of the few affected families in the world. Says a member of another such family: "It's been a disaster. A brutal suffering." Research on FFI began in 1984 when an Italian man named Silvano urged sleep scientists at the University of Bologna to discover "the cause of the curse of my family." Researchers watched as Silvano, 53, struggled to sleep while his body jerked him awake, preventing the restorative stage of sleep. A brain analysis later revealed two sections of his brain's switchboard, or thalamus, had been destroyed by abnormal prion proteins, affecting the sleep-wake cycle. For now, relatives can only undergo a genetic test and wait for the disease to hit, usually in their 50s. But Vallabh wants a different outcome. "The hope has to be always that you find a cure," says a pathologist, who imagines a time when "fatal" will be erased from FFI's name. The BBC reported last year on a drug that may keep abnormal prions from forming. (More on Vallabh and her husband here.)