David J. Loane, PhD

David Loane, PhD, is an Associate Professor and Faculty Member at the Shock, Trauma and Anesthesiology Research (STAR) Center 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 Associate 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 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 activation with the goal of manipulating these cells to attenuate destructive pro-inflammatory responses, and promote neuroprotective anti-inflammatory and reparative 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 anti-inflammatory activation 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.

Traumatic Brain Injury, Neuroinflammation, Microglia, Neuroprotection, Neurorepair, Chronic Neurodegeneration

1. Loane DJ, Deighan BF, Clarke RM, Griffin RJ, Lynch AM, Lynch MA.  Interleukin-4 mediates the neuroprotective effects of rosiglitazone in the aged brain. Neurobiology of Aging. 30 920-31, 2009.
2. Loane DJ, Pocivavsek A, Moussa CE-H, Thompson R, Matsuoka Y, Faden AI, Rebeck GW, Burns MP. APP secretases as therapeutic targets for traumatic brain injury. Nature Medicine. 15 377-9, 2009.
3. Kumar A, Stoica BA, Burns MP, Faden AI, Loane DJ. Traumatic brain injury in aged animals increases lesion size and chronically alters microglial/macrophage classical and alternative activation states. Neurobiology of Aging. 34 1397-411, 2013.
4. Loane DJ, Kumar A, Stoica BA, Cabatbat R, Faden AI. Progressive neurodegeneration after experimental brain trauma; association with chronic microglial activation. Journal of Neuropathology and Experimental Neurology. 73 14-29, 2014.
5. Kumar A, Barrett JP, Alvarez-Croda DM, Stoica BA, Faden AI, Loane DJ. NOX2 drives M1-like microglial/macrophage activation and neurodegeneration following experimental traumatic brain injury. Brain Behavior and Immunity. 58:291-309, 2016.
6. Barrett JP, Henry RJ, Villapol S, Stoica BA, Kumar A, Burns MP, Faden AI, Loane DJ. NOX2 deficiency alters macrophage phenotype through an IL-10/STAT3 dependent mechanism: implications for traumatic brain injury. J Neuroinflammation. 14:65, 2017.