Annelise Barron sits patiently at a small table in Stanford University’s Coupa Cafe, as freshly caffeinated college students mill around her. Thick stacks of paper sit close by — printouts of her recent studies on the body’s immune system. A small sticker adorns her laptop, reading “Bitcoin: because fuck banks.” It’s a hint at the bioengineer’s quirky tenacity, an essential quality if you’re going to cure Alzheimer’s disease, which is exactly what Barron aims to do.
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Alzheimer’s is the root cause of 60 to 80 percent of dementia cases, according to the Alzheimer’s Association, and the complexity of the disease has troubled neurology researchers for decades. But Barron, an associate professor of bioengineering at Stanford, has uncovered a way for our own immune system to fight off a major cause of Alzheimer’s. If her research leads to a treatment, it would be the first new therapeutics development in more than a decade.
Because Alzheimer’s is typically asymptomatic until it causes brain damage, clinical studies are incredibly challenging. The repeated failure of clinical trials led pharmaceutical giant Pfizer to drop out of Alzheimer’s research altogether in January.
These failures don’t faze Barron, whose take-charge mentality was honed as the third-oldest of 10 kids. Barron, 49, grew up in Fairbanks, Alaska, and Bellevue, Washington, primarily raised by her mom and stepdad. She’s also maintained a close relationship with her biological father, Carlos Barron, a Bolivian immigrant who fought for the U.S. in the Vietnam War. They share a mutual admiration, and although Barron married, she kept her maiden name, “for [her dad’s] sake, because I knew he was so proud of me.”
An aptitude for math and science led Barron to major in chemical engineering at the University of Washington and earn a Ph.D. at the University of California, Berkeley in the same field. She was the only woman in her class to finish the doctoral program. Her research hasn’t focused entirely on the end of life: Earlier this year, Barron developed a protein mimic for the creation of a synthetic lung surfactant (the coating that reduces surface tension in our lungs). The technology could help save the lives of some 20,000–30,000 babies born without fully developed lungs in the U.S. each year.
I want to show that the mechanism of Alzheimer’s disease is not what people think it is. A huge piece of the puzzle is missing.
While working at Northwestern University, Barron first became interested in the current focus of her Alzheimer’s research: peptides. These tiny proteins, made up of 50 amino acids or fewer, pack a wallop in several ways. For one, they can act as natural antibiotics in the body, attacking viruses or bacteria. Or they can regulate inflammation and the immune system. Over time, Barron and her team discovered that a peptide known as LL-37, which is part of our immune system, acts like an antidote to the peptide associated with Alzheimer’s disease, amyloid beta (Abeta). LL-37 may be able to neutralize Abeta’s harmful effects on the brain, and Barron is currently testing an oral combination therapy in mice that activates it in the brain and body.
But LL-37 can also be activated by natural means. “Exercising four times a week for 30 minutes, getting lots of sleep, eating salad and taking vitamin D are key to turning on this peptide,” Barron says. Prior therapeutics have all been aimed at ridding the body of Abeta, but Barron’s approach is completely different. “I want to show that the mechanism of Alzheimer’s disease is not what people think it is,” Barron says. “A huge piece of the puzzle is missing.”
Barron’s LL-37 research will publish later this year, and while she’s confident she’s onto something, a true cure for Alzheimer’s is likely to take years, if not decades. When using our own immunity to cure disease, “it’s important to make sure we’re not causing toxicity at the same time,” says David Holtzman, president of the American Neurological Association. When you target the immune system for treatment, it might protect you against one disease while causing another, he says. Holtzman agrees that there’s a lot of evidence showing the immune system is involved in staving off Alzheimer’s — but there are many unknowns.
And if the answer involves behavioral changes, we’re unlikely to find out anytime soon. Over the past five years, pharmaceutical companies including Merck, Axovant and Biogen have reported failures in clinical trials for Alzheimer’s treatment. Biogen and Eisai recently made progress on a potential Alzheimer’s drug, but their study is not yet peer-reviewed or published, and experts are treating it with cautious optimism. Without the promise of a miracle drug that can be sold for profit, there’s no incentive for Big Pharma to continue funding Alzheimer’s studies.
David Schwartz, professor of chemistry and genetics at the University of Wisconsin-Madison, doesn’t think that’ll stop Barron: “She could walk through rock.” The two scientists met 19 years ago at a Gordon Research Conference and have remained close friends. Schwartz says Barron’s background in chemical engineering allows her a unique understanding of both the physical and theoretical research in her field. She’s also proven resilient in the face of family strife. “Her trauma is unbelievable, but this woman is like a Timex watch — she just keeps ticking!” Schwartz says.
Barron has been married twice, and today is a single mother to three children — ages 16, 14 and 7. In 2013, she was charged with felony parent abduction when she took her kids to Hawaii and, she says, there was miscommunication with their father about the trip. All charges were eventually dropped, and her record is clear. “I’m just glad it’s over,” Barron says.
Advancing a career in bioengineering while raising three kids alone hasn’t been easy, but the promise of her research has been continually encouraging. “I want to solve big problems,” Barron says, “and I think we’re really onto something.” It’s her persistence, with a dash of a mad-scientist persona, that provides the faith that she can unlock a triumph where so many have failed.