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Alan I. Faden, MD

David S. Brown Professor in Trauma

Academic Title:

Professor

Primary Appointment:

Anesthesiology

Secondary Appointment(s):

Anatomy Neurobiology, Neurology, Psychiatry, Neurosurgery

Administrative Title:

Associate Dean, Trans-Campus Research Advancement

Additional Title:

Scientific Co-Director, Center for Brain, Health & Human Performance, University of Maryland (Baltimore and College Park)

Location:

MSTF 6-02

Phone (Primary):

(410) 706-4205

Fax:

(410) 706-7639

Education and Training

1966: University of Pennsylvania, Physics, BA, 1966

1967: Indiana University, History & Philosophy of Science, Graduate Studies

1971: University of Chicago School of Medicine, MD

1975: Resident, University of California-San Francisco, Neurology, 1974 (Chief Resident, 1975)

Biosketch

Dr. Faden is a neurologist who is an internationally recognized leader in neurotrauma. As the former director of the Center for Shock, Trauma and Anesthesiology Research (STAR), Dr. Faden oversaw multidisciplinary research focusing on brain injuries, critical care, and organ support, resuscitation, surgical outcomes, patient safety and injury prevention. He currently serves as the Scientific Co-Director for the bi-campus Center for Sports Medicine Health and Human Performance, as well as Associate Dean for Trans-Campus Research Advancement.

His present research focuses on the pathobiology and treatment of traumatic brain and spinal cord injuries, mechanisms of cell death, neuroinflammation, neuroimmunology, and brain systemic interactions. 

Research/Clinical Keywords

Traumatic Brain Injury (TBI), Neuroinflammation, Central Nervous System Injury, Neuroprotection, Cell Death and Recovery, Spinal Cord Injury, Neuroimmunology.

Highlighted Publications

 

 

Makarevich O, Sabirzhanov B, Aubrecht TG, et al. Mithramycin selectively attenuates DNA-damage-induced neuronal cell death. Cell Death Dis. 2020;11(7):587. Published 2020 Jul 27.

Li Y, Cao T, Ritzel RM, He J, Faden AI, Wu J. Dementia, Depression, and Associated Brain Inflammatory Mechanisms after Spinal Cord Injury. Cells. 2020;9(6):1420. Published 2020 Jun 8

Henry RJ, Meadows VE, Stoica BA, Faden A, Loane DJ. Longitudinal assessment of sensorimotor function following controlled cortical impact in mice: comparison of beamwalk, rotarod and automated gait analysis tests. J Neurotrauma. 2020 Jun 2. doi: 10.1089/neu.2020.7139. Online ahead of print. PMID: 32484024

 

Abulwerdi G, Stoica BA, Loane DJ, FADEN AI. Putative mGluR4 Positive Allosteric Modulators Activate Gi-Independent Anti-Inflammatory Mechanisms in Microglia. Neurochem Int. 2020 May 23:104770. doi: 10.1016/j.neuint.2020.104770. Online ahead of print. PMID: 32454165

Sabirzhanov B, Makarevich O, Barrett J, Jackson IL, Faden AI, Stoica BA. Down-Regulation of miR-23a-3p Mediates Irradiation-Induced Neuronal Apoptosis. Int J Mol Sci. 2020;21(10): E3695. 2020 May 24. PMID: 32456284

Cao T, Matyas JJ, Renn CL, Faden AI, Dorsey SG, Wu J. Function and Mechanisms of Truncated BDNF Receptor TrkB.T1 in Neuropathic Pain. Cells. 2020;9(5):E1194. 2020 May 11. PMID: 32403409

Doran SJ, Henry RJ, Shirey KA, Barrett JP, Ritzel RM, Lai W, Blanco JC, FADEN AI, Vogel SN, Loane DJ. Early or late bacterial lung infection increases mortality after traumatic brain injury in male mice and chronically impairs monocyte innate immune function. Crit Care Med. 2020 Mar 5. [Epub ahead of print] PMID: 32149839

Henry RJ, Ritzel RM, Barrett JP, Doran SJ, Jiao Y, Leach JB, Szeto GL, Stoica BA, FADEN AI, Loane DJ. Microglial depletion with CSF1R inhibitor during chronic phase of experimental traumatic brain injury reduces neurodegeneration and neurological deficits. J Neurosci . J Neurosci. 2020 Feb 24. pii: 2402-19. [Epub ahead of print] PMID: 32094203

Bhat SA, Henry RJ, Blanchard AC, Stoica BA, Loane DJ, Faden AI. Enhanced Akt/GSK-3β/CREB signaling mediates the anti-inflammatory actions of mGluR5 positive allosteric modulators in microglia and following traumatic brain injury in male mice. J Neurochem. 2020 Jan 11:e14954. doi: 10.1111/jnc.14954. [Epub ahead of print]

Barrett JR, Henry RJ, Shirey KA, Doran SJ, Makarevich OD, Ritzel RM, Meadows VA, Vogel SN, Faden AI, Stoica BA, Loane DJ. Interferon-β plays a detrimental role in experimental traumatic brain injury by enhancing neuroinflammation that drives chronic neurodegeneration. J of Neuroscience (in press)

Henry RJ,  Ritzel RM, Barrett JR, Doran SJ, Jiao Y, Leach JB, Szeto GL, Wu J, Stoica BA, Faden AI, Loane DJ.. Microglial depletion with CSF1R inhibitor during chronic phase of experimental traumatic brain injury reduces neurodegeneration and neurological deficits. J of Neuroscience (in press).

Doran SJ, Henry RJ, Shirey KA, Barrett JP, Ritzel RM, Lai W, Blanco JC, Faden AI, Vogel SN, and Loane DJ. Early or late bacterial lung infection increases mortality after traumatic brain injury in male mice and chronically impairs monocyte innate immune function. Critical Care Medicine 2020 (in press).

Henry RJ, Doran SJ, Barrett JP, Meadows VE, Sabirzhanov B, Stoica BA, Loane DJ, FADEN AI. Inhibition of miR-155 limits neuroinflammation and improves functional recovery after experimental traumatic brain injury in mice. Neurotherapeutics (in press)

Sabirzhanov B, Li Y, Coll-Miro M, Matyas JJ, He J, Kumar A, Ward N, Yu J, FADEN, AI, Wu J. Inhibition of NOX2 signaling limits pain-related behavior and improves, Motor function in male mice after spinal cord injury: participation of IL-10/miR-155 pathways. Brain Behav Immun. 2019 Feb 23. doi: 10.1016/j.bbi.2019.02.024

Kumar A, Henry RJ, Stoica BA, Loane DJ, Abulwerdi G, Bhat SA, FADEN AI. Neutral sphingomyelinase inhibition alleviates LPS-induced microglial activation and neuroinflammation after traumatic brain injury. J Pharmacol Exp Ther. 2019 Mar;368(3):338-352. doi: 10.1124/jpet.118.253955. Epub 2018

Additional Publication Citations

Faden, A.I., Demediuk P., Panter S.S., and Vink R., The role of excitatory amino acids and NMDA receptors in traumatic brain injury. Science 244 (4906): 798-800, 1989

Yakovlev, A.G., S.M. Knoblach, L. Fan, G.B. Fox, R. Goodnight, and Faden A.I. Activation of CPP32-like caspases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury. J Neurosci 17(19): 7415-24, 1997

Wu J, Zhao Z, Sabirzhanov B, Stoica BA, Kumar A, Luo T, Skovira J, Faden AI Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways. J Neurosci, 34(33):10989-11006, 2014

Sabirzhanov, B., Zhao, Z., Stoica, B.A., Loane D.J., Wu, J., Borroto, C., Dorsey, S., and Faden A.I., Down-regulation of miR-23a and miR-27a following experimental traumatic brain injury induces neuronal cell death through activation of pro-apoptotic Bcl-2 proteins. Journal of Neuroscience; 34 (30):10055-71, 2014

Kumar A, Stoica BA, Loane DJ, Yang M, Abulwerdi G, Khan N, Kumar A, Thom SR, FADEN AI. Microglial-derived microparticles mediate neuroinflammation after traumatic brain injury. J Neuroinflammation. 2017 Mar 15;14(1):47. PMID: 28292310

Matyas JJ, O'Driscoll CM, Yu L, Coll-Miro M, Daugherty S, Renn CL, FADEN AI, Dorsey SG, Wu J. Truncated TrkB.T1-mediated astrocyte dysfunction contributes to impaired motor function and neuropathic pain after spinal cord injury. J Neurosci. 2017 Apr 5;37(14):3956-3971. doi: 10.1523/JNEUROSCI.3353-16.2017. Epub 2017 Mar 7. PMID: 28270575

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 2017 Mar 24;14(1):65. doi: 10.1186/s12974-017-0843-4.PMID: 28340575

Ma EL, Smith AD, Desai N, Cheung L, Hanscom M, Stoica BA, Loane DJ, Shea-Donohue T, Faden AI. Bidirectional Brain-Gut Interactions and Chronic Pathological Changes after Traumatic Brain Injury in MIce. Brain Behav Immun. 2017 Jul 1. 2017 Nov; 66:56-69. doi: 10.1016/j.bbi.2017.06.018. Epub 2017 Jul 1. PMID: 28676351

Ritzel R, Doran S, Barrett J, Henry R, Ma E, FADEN A, Loane DJ. Chronic alterations of systemic immune function after traumatic brain injury. J Neurotrauma. 2018 Feb 8. doi: 10.1089/neu.2017.5399. [Epub ahead of print] PMID: 29421977

 

Research Interests

Alan I. Faden, M.D. is the David S. Brown Professor in Trauma in the Department of Anesthesiology. Dr. Faden’s laboratory uses multi-disciplinary approaches- including molecular and cellular biology, animal modeling, behavior, imaging and drug discovery- to examine the pathobiology of experimental brain and spinal cord injury and their treatment. Specific research focuses include neuroinflammation, cell death pathways, metabotropic glutamate receptors, extracellular vesicles, and brain systemic immunology interactions.

Awards and Affiliations

  • President, National Neurotrauma Society, 1988-89
  • President, San Francisco Neurological Society, 1990-91
  • President, American Society for Experimental NeuroTherapeutics (ASENT), 2006
  • Editor-in-Chief, Neurotherapeutics, 2003-2013
  • David S. Brown Professor, 2009
  • University Professor,  Kinesiology (Public Health,) University of Maryland, College Park, 2016

Links of Interest

Previous Positions

  • Dean of Research and Graduate Education, Medical Center, Georgetown University, Washington, DC, 1991-1996
  • Scientific Director, Medical Center, Georgetown University, Washington, DC, 1991-1996
  • Director, Georgetown Institute for Cognitive and Computational Sciences, Georgetown University, Washington, DC, 1995-1998
  • Professor of Neuroscience Neurology and Pharmacology, Georgetown University, Washington, DC, 1991-2009
  • Professor and Vice-Chair, Department of Neurology, University of California, San Francisco, 1984-1991
  • Chief, Neurology Service, Department of Veterans Affairs Medical Center, San Francisco, CA (1984-90)