Neuroscientist Stevens Named MacArthur 'Genius'

Research sheds light on nervous, immune systems interactions

HMS neuroscientist Beth Stevens talks about her research on the role of glia cells in the brain. Video: MacArthur Foundation

Beth Stevens, HMS assistant professor of neurology at Boston Children’s Hospital, has been named a 2015 MacArthur Fellow. She is among 24 individuals honored by the John D. and Catherine T. MacArthur Foundation for “pushing the boundaries of their fields.”

Fellows receive $625,000 paid out in installments over five years and are not evaluated or required to produce reports or products, making it a no-strings-attached award.

When Stevens began studying the role of glia in the brain in the 1990s, these cells—from the Greek for “glue”—weren’t given much thought. Traditionally, glia were thought to merely protect and support neurons, the brain’s real players.

But Stevens, whose lab is part of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital, has made the case that glia are key actors in the brain, not just caretakers. Her work—at the interface of the nervous and immune systems—is helping to transform how neurologic disorders like autism, amyotrophic lateral sclerosis (ALS), Alzheimer’s disease and schizophrenia are viewed.

Soon after college graduation in 1993, without prior experience in neuroscience, she helped discover an interplay between neurons and glial cells known as Schwann cells that control production of the nerve insulator myelin. It was one of the early pieces of evidence that glia and neurons “talk” to each other.

In 2007, while a postdoctoral fellow in the lab of Michael Greenberg, HMS Nathan Marsh Pusey Professor of Neurobiology and head of the Department of Neurobiology, Stevens showed how star-shaped glial cells called astrocytes influence the development of synapses, or brain connections. Studying neurons, her lab showed that a gene called C1q was markedly more active when astrocytes were present. C1q is an immune gene, one nobody had expected to see in a normal brain. In the context of disease, it initiates the complement cascade, an immunologic pathway for tagging unwanted cells and debris for clearance by other immune cells.

But in healthy developing brains, Stevens showed, C1q was concentrated at developing synapses, or brain connections, apparently marking certain synapses for pruning.

Then in 2012, the Stevens lab showed that microglia—another type of glia usually thought of as immune cells themselves—actively sculpt the brain’s wiring. They literally trim away unwanted, inappropriate synapses by eating them—in the same way they would engulf and destroy invading bacteria.

That paper was cited by the journal Neuron as their most influential paper of 2012.

The same year, Stevens was one of the recipients of the Presidential Early Career Awards for Scientists and Engineers honoring her innovative research and scientific leadership.

Stevens is currently investigating synapse loss—a hallmark of neurodegenerative conditions such as Alzheimer’s—and trying to understand why it occurs. Her lab’s recent work suggests that normal pruning mechanisms that are active during early brain development get re-activated later in life. Intervening in this activation could lead to a new treatment approach, she believes.

Adapted from Boston Children’s Vector blog.