Beth Stevens is an assistant professor in the Department of Neurology at Harvard Medical School and the F. M. Kirby Neurobiology Center at Boston Children’s Hospital.
Education
Beth Stevens received a Bachelor of Surgery (1993) from Northeastern University, and a Doctor of Philosophy in Neuroscience in 2003 from the University of Maryland, College Park. She completed her postdoctoral fellowship at the Stanford University School of Medicine in 2008.
Career
She has helped to identify the role of microglia in the “pruning” or removal of synaptic cells during brain development and has also determined that the impaired microglial function and abnormal activation of this pruning pathway could be responsible for diseases like autism, schizophrenia, and Alzheimer"son In 2012, Stevens’ team published evidence that microglia "eat" synapses, especially those that are weak and unused. The findings pinned down a new role for microglia in wiring the brain, indicating that adult neural circuitry is determined not only by the nerve cells but also by the brain’s immune cells, and helped to explain how the brain, which starts out with a surplus of neurons, trims some of the excess away.
Neuron named the paper its most influential publication of 2012.
She continues to study the function of microglia in the healthy brain, most recently uncovering preliminary evidence that a certain protein serves as a ‘don’t eat me’ tag that protects synapses from being engulfed by microglia. She received a MacArthur Fellowship in 2015.
Stevens is exploring the role of microglia in disorders such as autism. Several studies suggest that microglia are more active and more numerous in the brains of people with autism than in controls, and Stevens and her team are looking at whether the activity of microglia is altered during brain development in mouse models of autism.
Her work suggests that adult diseases caused by deficient neural architecture (such as autism and schizophrenia) or states of neurodegeneration (such as Alzheimer’s or Huntington’s disease) may be the result of impaired microglial function and abnormal activation of the pruning pathway.