Stephen A. Back, MD, PhDScientific Advisory Board, Member
Stephen A. Back, MD, PhD
Oregon Health Sciences University
Areas of Specialty: Dr. Back is a board certified neurologist, specializing in developmental neurobiology and pediatric neurology. His expertise includes the etiology of brain injury in premature infants, including cerebral palsy and cerebral white matter injury.
Research Activities: Dr. Back’s research focuses on developing novel strategies to repair and regenerate injuries in the developing brain, particularly in survivors of preterm birth. Dr. Back investigates the causes of cerebral palsy (CP), studying the mechanisms by which hypoxia-ischemia (insufficient brain oxygenation caused by low blood flow) generates cerebral white matter injury, the major cause of CP. His laboratory employs multiple research approaches, including human tissues, tissue culture systems, and animal models, and extends these findings to adult disorders such as multiple sclerosis and Alzheimer’s disease. The primary objective of Dr. Back’s lab is to define cellular and molecular mechanisms associated with developmental brain injuring through the combination of pediatric neurology and developmental biology. Dr. Back gained international recognition for identifying the oligodendrocyte progenitor as the predominant cell type killed in cerebral white matter as a result of premature birth, and has received multiple prestigious awards for this work. His research is supported by the American Heart Association, the National Institute of Neurologic Disorders and Stroke, and the Child Neurology Society. As a clinician-scientist with expertise in pediatric neurology and proven dedication to child care, Dr. Back brings vital experience to the SmartTots Scientific Advisory Board.
Scientific Advisory Board, Member
Oregon Health & Sciences University (OHSU)
Associate Professor of Pediatrics, Neurology and Anesthesiology
OHSU Doernbecher Children’s Hospital
Director, Pediatric Brain Injury Research Laboratory
University of California, Irvine – MD, PhD, Pharmacology (1990)
Pediatrics Residency, University of California, Irvine Medical Center
Pediatric Neurology Fellowship, Harvard Medical School
Recent Research Funding
Cellular Mechanisms of Fetal White Matter IndustryNational institute of Neurological Disorders and Stroke (2007-2011)Principal Investigator
- Javits Neuroscience Investigator Award, National Institute of Neurological Disorders and Stroke
- Young Investigator Award, Child Neurology Society
- Bugher Award, American Heart Association
Q & A
Buser JR, Segovia KN, Dean JM, Nelson K, Beardsley D, Gong X, Luo NL, Ren J, Wan Y, Riddle A, McClure MM, Ji X, Derrick M, Hohimer AR, Back SA, Tan S.Timing of appearance of late oligodendrocyte progenitors coincides with enhanced susceptibility of preterm rabbit cerebral white matter to hypoxia-ischemia. J Cereb Blood Flow Metab 2010;30(5):1053-65.
Back SA, Craig A, Kayton R, Luo NL, Meshul CK, Allcock N, Fern R. Hypoxia-ischemia preferentially triggers glutamate depletion from oligodendroglia and axons in perinatal cerebral white matter. J Cereb Blood Flow Metab 2007;27:334-347.
Back SA, Riddle A, McClure MM. Maturation-dependent vulnerability of perinatal white matter in premature birth. Stroke 2007;38(2):724-30.
Back SA, Craig A, Ribiero I, Stewart W, Rivkees SA. Protective effects of caffeine on chronic hypoxia-induced cerebral white matter injury. Ann Neurol 2006;60(6):696-705.
Derrick M, Luo NL, Bregman JC, Jilling T, Ji X, Fisher K, Gladson CL, Beardsley DJ, Murdoch G, Back SA, Tan S. Preterm fetal hypoxia causes hypertonia and motor deficits in the neonatal rabbit: a model for human cerebral palsy? J Neurosci 2004;24(1):24-34.
Back SA, Luo NL, Borenstein NS, Levine JM, Volpe JJ, Kinney HC. Late oligodendrocyte progenitors coincide with the developmental window of vulnerability for human perinatal white matter injury. J Neurosci 2001;21(4):1302-1312.