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UCLA Neurosurgery


David Hovda, PhD

David Hovda, PhD

Dr. Hovda


Professor and Vice Chairman of Research Affairs
Director, UCLA Brain Injury Research Center
Lind Lawrence Eminent Scholar





Hospital Affiliation

Ronald Reagan UCLA Medical Center
David Geffen School of Medicine at UCLA
UCLA Neurosurgery
Box 956901
Los Angeles, CA 90095-6901




  • B.S., Psychology, University of New Mexico, Albuquerque, NM (1979)
  • M.S., Psychobiology, University of New Mexico, Albuquerque, NM (1982)
  • Ph.D., Psychology, University of New Mexico, Albuquerque, NM (1985)
  • Postdoctoral Fellowship, Neurophysiology, University of California at Los Angeles, CA (1987)


In 1989, Dr. Hovda was recruited by the Department of Neurosurgery to direct its scientific efforts to understand the cellular pathophysiology of brain injury. This work resulted in providing the backbone for UCLA being recognized as a "Center of Excellence" by the National Institutes of Health.He has devoted most of his career to understanding the mechanisms of recovery of function. Dr. Hovda is the Director of the UCLA Brain Injury Research Center. He is a former President and current President - Elect of the National Neurotrauma Society and study section committee chair for the National Institute for Neurological Disease and Stroke (NINDS). He is the current chair for the Brain Injury and Neurovascular Pathologies study section for the NINDS and has been elected President of the International Neurotrauma Society (2009-2012). Dr. Hovda has received a number of awards for his research on brain injury and recovery of function, including the 1991 National Head Injury Foundation Award, the Giannini Foundation Award, the Benjamin Franklin Haught Memorial Award and named the Lind Lawrence Eminent Scholar for his work on the topic of Traumatic Brain Injury. In addition Dr. Hovda received the 2006 Women in Neurotrauma award for his teaching and support for women in neuroscience. Dr. Hovda is most well known internationally for his translational work on the pathobiology of traumatic brain injury.


  • R01 (NS045804) Gómez-Pinilla (PI) 12/01/04 – 11/30/09 Role: Co-Investigator
    NINDS/NIH Division of Stroke and Trauma
    “Activity-Induced Recovery Following Brain Trauma”
    To determine if reduced cognitive capacity following TBI is the result of dysfunction in the molecular mechanisms that support synaptic plasticity.
  • R01 (NS050465-01) Gómez-Pinilla (PI) 7/01/05 – 6/30/10
    NINDS/NIH Division of Stroke and Trauma
    “Restoration of Homeostasis After Brain Trauma”
    The major goals of this project are to determine mechanisms involved in oxidative stress and energy crisis in traumatic brain injury, and the possibility to modulate free radical formation by restoring brain homeostasis.
  • R21 (NS048535-01A1) Griesbach (PI) 4/01/05 – 3/31/07 Role: Co-Investigator
    NINDS/NIH Division of Stroke and Trauma
    “Voluntary Exercise Therapy After Traumatic Brain Injury”
    To determine whether voluntary exercise up-regulates BDNF following traumatic brain injury.
  • R01 (NS052406-01) Prins (PI) /01/05 – 6/30/08 Role: Co-Investigator
    NINDS/NIH Division of Stroke and Trauma
    “Age-Dependent Ketone Metabolism After Brain Injury”
    To determine the use of ketone bodies as an alternate metabolic substrate following traumatic brain injury in the developing brain.
  • R01 (NS049471) Vespa (PI) 1/01/06 – 12/31/10 Role: Co-Investigator
    NINDS/NIH Division of Stroke and Trauma
    “MRS Detects Metabolic Dysfunction after Brain Injury”
    This application focuses on the consequences of traumatic brain injury on the human brain to utilize oxygen. Traditional measurements of the cerebral metabolic rates for oxygen will be compared to magnetic resonance spectroscopy to determine the degree of mitochondrial dysfunction as it relates to posttraumatic atrophy.
  • R01 (NS 027544-10) Hovda (PI) 1/19/06 – 12/31/09 Role: Principal Investigator
    NINDS/NIH Division of Stroke and Trauma
    “Loss of Developmental Plasticity Following Head Injury”
    The primary goal of this project is to characterize the morphological, behavioral and molecular response to traumatic injury in the immature brain as it relates to enriched environment-induced experience-dependent plasticity.




1992-Present Lind Lawrence Eminent Scholar
1992-1994 The National Head Injury Foundation Young Investigator Award
1987 Giannini Foundation Postdoctoral Scholar

PUBLICATIONS (recent articles)

  1. Controlled contusion injury alters molecular systems associated with cognitive performance. Griesbach GS, Sutton RL, Hovda DA, Ying Z, Gomez-Pinilla F. J Neurosci Res. 2008 Oct 1. [Epub ahead of print]
  2. The impact of substance abuse on mortality in patients with severe traumatic brain injury. O'Phelan K, McArthur DL, Chang CW, Green D, Hovda DA. J Trauma. 2008 Sep;65(3):674-7.
  3. Persistent metabolic crisis as measured by elevated cerebral microdialysis lactate-pyruvate ratio predicts chronic frontal lobe brain atrophy after traumatic brain injury. Marcoux J, McArthur DA, Miller C, Glenn TC, Villablanca P, Martin NA, Hovda DA, Alger JR, Vespa PM. Crit Care Med. 2008 Oct;36(10):2871-7.
  4. Duration of ATP reduction affects extent of CA1 cell death in rat models of fluid percussion injury combined with secondary ischemia. Aoyama N, Lee SM, Moro N, Hovda DA, Sutton RL. Brain Res. 2008 Sep 16;1230:310-9. Epub 2008 Jul 9.
  5. Voluntary exercise or amphetamine treatment, but not the combination, increases hippocampal brain-derived neurotrophic factor and synapsin I following cortical contusion injury in rats. Griesbach GS, Hovda DA, Gomez-Pinilla F, Sutton RL. Neuroscience. 2008 Jun 23;154(2):530-40. Epub 2008 Apr 9.
  6. Time window for voluntary exercise-induced increases in hippocampal neuroplasticity molecules after traumatic brain injury is severity dependent. GS, Gómez-Pinilla F, Hovda DA. J Neurotrauma. 2007 Jul;24(7):1161-71.
  7. The fate of glucose during the period of decreased metabolism after fluid percussion injury: a 13C NMR study. Bartnik BL, Lee SM, Hovda DA, Sutton RL. J Neurotrauma. 2007 Jul;24(7):1079-92.
  8. Pericontusional brain tissue exhibits persistent elevation of lactate/pyruvate ratio independent of cerebral perfusion pressure.
    Vespa PM, O'Phelan K, McArthur D, Miller C, Eliseo M, Hirt D, Glenn T, Hovda DA. Crit Care Med. 2007 Apr;35(4):1153-60.
  9. Increased pentose phosphate pathway flux after clinical traumatic brain injury: a [1,2-13C2]glucose labeling study in humans. Dusick JR, Glenn TC, Lee WN, Vespa PM, Kelly DF, Lee SM, Hovda DA, Martin NA. J Cereb Blood Flow Metab. 2007 Sep;27(9):1593-602.
  10. Glucose metabolism after traumatic brain injury: estimation of pyruvate carboxylase and pyruvate dehydrogenase flux by mass isotopomer analysis. Bartnik BL, Hovda DA, Lee PW. J Neurotrauma. 2007 Jan;24(1):181-94.

Read my PubMed publications


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