Lindsay De Biase, Ph.D.

Research Interests

Lindsay M. De Biase received her B.S. in Molecular, Cellular, and Developmental Biology from Yale University in 2003. She then worked for 2 years with Dr. Eric Hoffman as a research assistant at the Children’s National Medical Center in Washington D.C. where she used microarray-based approaches to study gene expression of myocytes in mouse models of amyotrophic lateral sclerosis and designed new protocols to purify peripheral immune cells for analysis of gene expression during acute lung injury. Lindsay began graduate work with Dr. Dwight Bergles at Johns Hopkins School of Medicine in 2005 and earned her Ph.D. in Neuroscience in 2011. Her graduate work used slice electrophysiology and imaging-based approaches to study synaptic signaling between neurons and cells of the oligodendrocyte lineage and suggested key roles for this signaling in regulating maturation of oligodendrocyte precursor cells. Lindsay continued to focus on neuron-glial interactions as an IRTA Postdoctoral Fellow in the laboratory of Dr. Antonello Bonci in the Synaptic Plasticity Section of the Cellular Neurobiology Branch beginning in 2012. Her research has focused on microglial cells, a dynamic, versatile, macrophage-like population of cells within the CNS that are understudied in brain regions affected by drugs of abuse. Using a combination of imaging, electrophysiology, and transcriptome sequencing, she discovered that microglia in distinct nuclei of the basal ganglia (BG) exhibit striking differences in basic properties and functional states, overturning the widespread assumption that these cells are equivalent throughout the CNS. Lindsay recently accepted a position as Assistant Professor in the Department of Physiology at UCLA and, in her own lab, will continue to study the mechanisms that give rise to microglial regional specialization and its impact on BG neuronal function and microglial responses to pathology. This work will provide valuable insight into how microglia inform neuronal function and viability and yield novel strategies for therapeutic manipulation of microglial phenotype in pathological contexts that affect the basal ganglia.