Boston Children's Researcher Spotlight:
Beth Stevens, PhD, Investigator in the F.M. Kirby Neurobiology Center
In this monthly new showcase, TIDO will highlight an up and coming researcher within the Boston Children's community by asking the researcher three questions about their research. This month, we had the pleasure of interviewing neuroscientist Beth Stevens, PhD. Research in the laboratory of Dr. Stevens seeks to understand how neuron-glia communication facilitates the formation, elimination and plasticity of synapses—the points of communication between neurons—during both healthy development and disease.
Beth Stevens, PhD
Q: What drives you as a scientist?
Beth: Pure curiosity, the thrill of discovery and the desire to figure out how synaptic connections are formed and lost. I am gaining interest in seeing how some of my lab’s basic scientific discoveries related to microglia function and synapse elimination can translate to CNS diseases. Our most recent work has put us at the exciting interface between the nervous and immune system. My interactions with BCH immunologists and those in other fields who continually offer different perspectives are guiding the future of my research.
Q: What is unique about your research?
Beth: The emerging idea that immune molecules, such as complement, are expressed in the healthy brain and function at synapses was unexpected and raises many mechanistic questions. Until recently, microglia were primarily studied in the context of disease and inflammation. Our finding that microglia mediate synaptic pruning during normal development has changed the way we think about these fascinating glial cells. Our research suggests microglia play an active role in the pruning process rather than cleaning up synaptic debris. Ongoing efforts are underway to understand how microglia are talking to and ‘listening’ to synapses and to identify protective and ‘punishment’ molecules that regulate synaptic pruning.
My lab is also interested in understanding the potential link between microglia and immune dysfunction and neurodevelopmental disorders (NDDs) such as Rett syndrome and autism. Understanding the normal function of microglia is likely to provide key insight into this link and may lead to new therapeutic targets.
Q: What unmet needs does your research aim to solve?
Beth: Early synapse loss and dysfunction are increasingly recognized as a hallmark of Alzheimer’s disease and other NDDs. It is now clear that synapse loss occurs long before cell death and pathology so it is critical to identify biomarkers and treatments for early intervention of NDDs.
A major question we are attempting to answer is what makes synapses and certain brain regions more vulnerable to NDDs? My lab has identified novel mechanisms that drive synapse elimination during neural development, which is providing important clues. Our ongoing work aims to test the hypothesis that similar mechanisms are reactivated to trigger early synapse loss in NDDs and develop strategies to protect synapses.