Beth Stevens, Ph.D.

Associate Professor of Neurology
Harvard Medical School
Boston Children's Hospital

Member, Broad Institute

Beth Stevens is an associate professor at Harvard Medical School in the FM Kirby Neurobiology Center at Boston Children’s Hospital and an institute member of the Broad Institute.

Her research seeks to understand the mechanisms that regulate the development and elimination of synapses by focusing on how microglia and immune-related molecules mediate this process.

Beth received her Ph.D. in neuroscience in 2003 at the University of Maryland, College Park. She performed her dissertation research at the National Institutes of Health (NICHD) in the area of neuron-glia interactions. In her postdoctoral work with Ben Barres at Stanford University, she discovered that the classical complement cascade, part of the innate immune system, helps to mediate developmental CNS synapse elimination. Their findings have raised many questions about how the complement cascade normally works to eliminate synapses and especially whether it becomes abnormally reactivated in brain diseases such as Alzheimer’s disease (AD) that impair synaptic connectivity. In 2008, Dr. Stevens established her independent laboratory in the FM Kirby Neurobiology Center at Children’s Hospital, where she is currently using a combination of molecular, physiological and high-resolution imaging techniques to dissect the mechanisms by which microglial cells and immune-related molecules (i.e. complements, cytokines) regulate synapse function during health and disease. She is investigating the mechanisms that drive synapse loss and dysfunction in AD and Huntington’s disease, as well as neurodevelopmental disorders, such as autism and schizophrenia. Beth is a recipient of several young investigator awards, including the Ellison Medical Foundation New Scholar in Aging, John Merck Scholar (2011), Presidential Early Career Award for Scientists and Engineers (PECASE), and a MacArthur Award.

Funded Research

Project Description Researchers Funding
Early Role of Microglia in Synapse Loss in Alzheimer’s Disease

In Alzheimer’s disease (AD), synaptic connections are lost early and in specific areas of the brain, including the hippocampus, where memory is formed and stored; however, what makes synapses vulnerable in AD and other neurodegenerative diseases remains elusive. In the healthy developing brain, synaptic loss (also known as synaptic pruning) is a normal process required for proper brain development. We previously found a key role for a group of immune molecules called complement in synaptic pruning.

2016 to 2017

$300,000