David Loane, PhD, is an Assistant Professor of Anesthesiology and Faculty Member at the Center for Shock, Trauma and Anesthesiology Research (STAR) at the University of Maryland School of Medicine, Baltimore, Maryland. Dr. Loane conducted his graduate studies at the Department of Pharmacology and MRC Center for Synaptic Plasticity, University of Bristol, England, and obtained his PhD in Neuroscience in 2005. He then pursued postdoctoral training with Dr. Marina Lynch at Trinity College Institute of Neuroscience, Trinity College Dublin, Ireland, where he studied neuroinflammatory changes in the aged and Alzheimer's disease (AD) brain. In 2007 Dr. Loane was recruited to the Department of Neuroscience, Georgetown University Medical Center, Washington D.C., to perform further postdoctoral training on experimental models of traumatic brain injury (TBI) under the mentorship of Dr. Alan Faden. He joined the faculty of the University of Maryland School of Medicine in November 2009 and is currently Assistant Professor of Anesthesiology.
Dr. Loane leads a multi-disciplinary research team dedicated to studying the complexities of TBI, neuroinflammation and tissue repair. Specifically, his research program investigates the activation status and functional role of resident microglia and infiltrating blood-borne monocytes (macrophages) in the TBI brain, and to determine how they contribute to chronic neurodegeneration and long-term neurological dysfunction after brain trauma. His group is seeking to elucidate the mechanisms that regulate microglial/macrophage polarization (M1/M2 activation states) with the goal of manipulating these cells to attenuate destructive pro-inflammatory (M1) responses, and promote protective repair (M2) responses. Ongoing studies include examining: 1) the function and phenotypes of microglia/macrophages following acute TBI, and how they contribute to chronic pathologies; 2) the signaling pathways that drive M2 polarization of microglia/macrophages, and whether these pathways can be manipulated after TBI; 3) how age affects microglia/macrophage polarization and the neuroinflammatory response after TBI. The mission of his group is to elucidate the pathophysiological mechanisms underlying post-traumatic neuroinflammation, neurodegeneration and loss of neurological function, and to develop novel treatment strategies that will translate to the clinic for human head injury.
Microglial Activation Phenotypes and Mechanisms of Repair in the Aged TBI Brain
The Effect of Voluntary Exercise on Microglial Activation Phenotypes in the Aged Injured Brain