That dedication to scientific truth above careerism — his openness didn’t endear him to the powers that be — defined his professional life. When he died in the early hours of Friday of glioblastoma at only 58, Moir, an assistant professor of neurology at Massachusetts General Hospital and Harvard Medical School, left a legacy of brilliant science: His idea that Alzheimer’s has something to do with microbes in the brain, that amyloid plaques form in defensive response to those pathogens, and that something besides eliminating amyloid is probably our best shot at preventing or treating Alzheimer’s.

Scientists before him had the same hunch, but Moir amassed arguably the strongest evidence for it. That all became part of my 2018 story. But so did his saga of struggling for National Institutes of Health funding and clashing with journal editors scared to publish anything outside the mainstream.

Moir shared with STAT the score sheets for his NIH grant requests and the rejections from journals. One NIH reviewer panned him for wanting to study something (a microbial origin for Alzheimer’s) that hadn’t been proved; it wasn’t a good look for a process that’s supposed to be all about discovering new knowledge. Another sneered that Moir was a mere assistant professor, as if rank trumped merit in deciding what research to fund. A top journal almost published a key paper of his, but backed down when its Alzheimer’s experts (read: defenders of Alzheimer’s orthodoxy) panned it.

When that research was finally published in 2016, showing that amyloid is part of an immune response to brain microbes, it was voted one of the top five discoveries in neurology that year.

“It shouldn’t have been so difficult for him to get the support and recognition that he deserves,” Moir’s wife, Julie Alperen, told me soon before his death.

Maybe it was his humble background that gave Moir the courage to follow the science and not the crowd, damn the career consequences. He grew up on a farm in the middle of nowhere in western Australia and didn’t learn to read or write until he was 12. Compared to where he might have wound up, being punished for questioning Alzheimer’s orthodoxy was nothing.

“Rob was always a dogged researcher, meaning like a dog with its bone,” Colin Masters, the distinguished Alzheimer’s researcher at the University of Melbourne who trained Moir, told me for the 2018 story. “He never gives up and has never been one to follow the standard line.” His mentor, Mass. General’s Rudolph Tanzi, called him “the most out-of-the-box thinker I’ve ever met — in any field. He doesn’t even see the box.”

When I asked Moir where he got his anti-establishment streak, he mentioned taking a microbiology course from future Nobel laureate Barry Marshall, who bucked orthodoxy for years by arguing that a bacterial infection (H. pylori) causes ulcers. “Everyone thought he was crazy,” Moir recalled last year. “He was crazy, but he was also right.”

Although Moir was known for the microbial hypothesis of Alzheimer’s, he was sort of a Forrest Gump of Alzheimer’s, at the center of some of the field’s key moments. A 2005 study he led identified natural antibodies against the Alzheimer’s-defining protein fragment beta-amyloid; a similar lab-made antibody, aducanumab, might become the first successful anti-amyloid Alzheimer’s drug. And while the consensus of Alzheimer’s researchers is that a protein called apoE acts by clearing amyloid or failing to do so, Moir believed apoE seeds amyloid.

“He was the first person to suggest that,” Tanzi said. “I guarantee you, that idea will be rediscovered” and inspire Alzheimer’s treatments.

Harvard took the boy out of Australia, but it couldn’t keep Australia out of the Mass. General lab. Moir regularly had colleagues in hysterics over his off-color jokes (many involving sheep) and tales of growing up in his country’s desolate west (such as when he saved a pet duck from becoming dinner). One day, to illustrate what he meant by apoE seeding amyloid, he pulled out his ratty old leather wallet and its patina of salt crystals. To explain how it mimics amyloidosis, he began by telling his colleagues, “Dude, the sweat from my butt is hitting the leather, and then …”

Just as STAT’s profile of Moir was about to run, he called to say he’d heard from NIH. The agency had found some extra money in its budget. Would he please respond to the last round of reviewers, who had rejected his grant proposal, and resubmit it? He did. He received $3.2 million in 2019 to support research in mice and in human neurons growing on lab plates (“Alzheimer’s in a dish”) examining whether herpes or other viruses in the brain can exacerbate the buildup of both amyloid and tau, a neuron-killing protein fragment that’s also found in Alzheimer’s brains.

His lab has continued to function during his illness and the research will be completed by his students, overseen by Tanzi.