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Alan I. Faden, MD

David S. Brown Professor of Trauma

Academic Title:


Primary Appointment:


Secondary Appointment(s):

Neurosurgery, Neurobiology, Neurology, Psychiatry

Administrative Title:

Associate Dean, Trans-Campus Research Advancement


MSTF 6-02

Phone (Primary):

(410) 706-4205


(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)


Dr. Faden is a neurologist who is an internationally recognized leader in neurotrauma. He served as the initial director of the Center for Shock, Trauma and Anesthesiology Research (STAR), Co-Director for the bi-campus Center for Brain, Health and Human Performance, and Associate Dean for Trans-Campus Research Advancement.

From 1991-2009, he was Professor of Neuroscience, Neurology, and Pharmacology at Georgetown University, where he served as Dean for Research, Scientific Director of the Medical Center, and inaugural Director of Georgetown Institute for Cognitive and Computational Sciences (GICCS). From 1984-1991 he was Professor and Vice Chair of Neurology at UCSF, Chief of Neurology at the San Francisco VA Medical Center, and Director of the Center for Neural Injury. Dr. Faden has published 415 refereed research papers, 50 book chapters and proceedings, and 10 books/monographs.  His brain injury and spinal cord injury research programs have each received continuous NIH support for more than 30 years. He was founding Editor-in-Chief of Neurotherapeutics and founding Associate Editor of the Journal of Neurotrauma.  Dr. Faden served as President of the American Society for Experimental NeuroTherapeutics, first President the National Neurotrauma Society, and President of the San Francisco Neurological Society. He has received the Exceptional Service Medal from the Uniformed Services University and the Distinguished Service Award from the University of Chicago.

His interdisciplinary research focuses on modeling, behavior, neuropathology, immunology, cell biology and molecular biology, including single cell transcriptomics and epigenetics. It focuses on the pathobiology and treatment of traumatic brain and spinal cord injuries, mechanisms of cell death and dementia, neuroinflammation, neuroimmunology, and bidirectional brain systemic interactions. 

Research/Clinical Keywords

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

Highlighted Publications

Faden AI, Holaday JW. Opiate antagonists: a role in the treatment of hypovolemic shock. Science. 1979;205(4403):317-8. PMID: 451606.

Faden AI, Jacobs TP, Holaday JW. Thyrotropin-releasing hormone improves neurologic recovery after spinal trauma in cats. N Engl J Med. 1981;305(18):1063-7. PMID: 6792542.

Faden AI, Jacobs TP, Holaday JW. Opiate antagonist improves neurologic recovery after spinal injury. Science. 1981;211(4481):493-4. PMID: 7455690.

Faden AI, Simon RP. A potential role for excitotoxins in the pathophysiology of spinal cord injury. Ann Neurol. 1988:23(6):623-6. PMID: 2841902.

Faden AI, Demediuk P, Panter SS, Vink R. The role of excitatory amino acids and NMDA receptors in traumatic brain injury. Science. 1989:244(4906):798-800. PMID: 2567056.

Pitts LH, Ross A, Chase GA, Faden AI. Treatment with thyrotropin-releasing hormone (TRH) in patients with traumatic spinal cord injuries. J Neurotrauma. 1995;12(3):235-43. PMID: 7473798.

Yakovlev AG, Knoblach SM, Fan L, Fox GB, Goodnight R, Faden AI. Activation of CPP32-like caspases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury. J Neurosci. 1997;17(19):7415-24. PMID: 9295387.

Di Giovanni S, Movsesyan V, Ahmed F, Cernak I, Schinelli S, Stoica B, Faden AI. Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury. Proc Natl Acad Sci USA. 2005;102(23):8333-8. PMID: 15923260.

Di Giovanni S, Knights CD, Rao M, Yakovlev A, Beers J, Catania J, Avantaggiati ML, Faden AI. The tumor suppressor protein p53 is required for neurite outgrowth and axon regeneration. EMBO J. 2006;25(17):4084-96. PMID: 16946709.

Loane DJ, Pocivavsek A, Moussa CE, Thompson R, Matsuoka Y, Faden AI, Rebeck GW, Burns MP. Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury. Nat Med. 2008;15(4):377-9. PMID: 19287391.

Piao CS, Stoica BA, Wu J, Sabirzhanov B, Zhao Z, Cabatbat R, Loane DJ, Faden AI. Late exercise reduces neuroinflammation and cognitive dysfunction after traumatic brain injury. Neurobiol Dis. 2012;54,252-63. PMID: 23313314.

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. 2014;34(33):10989-1006. PMID: 25122899.

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. 2016;14(1):47. PMID: 28292310.

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;66:56-69. PMID: 28676351         

Henry RJ, Ritzel RM, Barrett JP, 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 Neurosci. 2020;40(14):2960-2974. PMID: 32094203.

Khan NZ, Cao T, He J, Ritzel RM, Li Y, Henry RJ, Colson C, Stoica BA, Faden AI, Wu J. Spinal cord injury alters microRNA and CD81+ exosome levels in plasma extracellular nanoparticles with neuroinflammatory potential. Brain Behav Immun. 2021;92, 165-183. PMID: 33307173.

Hanscom M, Loane DJ, Aubretch T, Leser J, Molesworth K, Hedgekar N, Ritzel RM, Abulwerdi G, Shea-Donohue T, Faden AI. Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits. J Neuroinflammation. 2021;18(1):24. PMID: 33461596.

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)
  • Director, Shock, Trauma and Anesthesiology Research (STAR) Organized Research Center, University of Maryland, Baltimore, 2009-2019
  • Co-Director, Center for Brain, Health & Human Performance, University of Maryland (Baltimore and College Park), 2017-2022