Clinical Investigations Section - Division of Intramural Research

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John M. Hallenbeck Image

 John M.  Hallenbeck  M.D., Senior Investigator

Dr. Hallenbeck received his M.D. degree from the University of Pennsylvania. After a medical internship and neurology residency at the University of Michigan, he entered the United States Navy. At the Naval Medical Research Institute his research focused on CNS decompression sickness and air embolism and later the study of inflammatory and immune mechanisms in acute brain ischemia. In 1983, he was appointed Chief of the Navy's neurology training program at the National Naval Medical Center and Professor, Vice-Chairman and Chairman for Research in the Department of Neurology, Uniformed Services University of the Health Sciences. In 1991 he came to the NINDS as Chief of the newly created Stroke Branch. He received the Mihara Cerebrovascular Disorder Research Prize. Dr. Hallenbeck's laboratory is studying the cellular regulation of ischemic tolerance and inflammatory and immune mechanisms in the initiation and progression of stroke.

Laboratory Staff

Tahir Ahmed, , Predoctoral Fellow , 301-443- 3424
Paola Castri, M.D., Ph.D., Visiting Fellow
Bolanle Famakin, M.D., Clinical Fellow , 301-402- 6936
Dace Klimanis, M.Sc, Research Assistant , 301-402- 2338
Yang-Ja Lee-Wickner, Ph.D., Staff Scientist , 301-402- 6939
Xinhui Li, Ph.D., Post-Doctoral IRTA , 301-435- 6559
David McMullen, Ph.D., Visiting Fellow , 301-451- 6585
Yongshan Mou, M.D., Senior Research Fellow , 301-594- 2597
Christl Reutzler, B.A., Research Assistant , 301-496- 8111
Maria Spatz, M.D., Special Volunteer , 301-496- 8111



Research Interests

The Clinical Investigations Section of the Stroke Branch conducts translational research on stroke prevention and stroke treatment. In spontaneously hypertensive, stroke-prone rats, we are studying ways of preventing development of spontaneous brain infarcts. This work is focused on immunologic approaches that suppress the endothelial activation produced by inflammatory cytokines such as TNF and IL-1. Mucosal tolerization to E-selectin targets immunomodulation to vascular segments that are becoming activated and suppresses spontaneous strokes and hemorrhages. This work is being translated into clinical trials.

Selected Recent Publications

Lee YJ, Castri P, Bembry J, Maric D, Auh S, Hallenbeck JM
SUMOylation participates in induction of ischemic tolerance - J Neurochem  109 257-67 2009

Ishibashi S, Maric D, Mou Y, Ohtani R, Ruetzler C, Hallenbeck JM
Mucosal tolerance to E-selectin promotes the survival of newly generated neuroblasts via regulatory T-cell induction after stroke in spontaneously hypertensive rats - J Cereb Blood Flow Metab  29 606-20 2009

Wakita H, Ruetzler C, Illoh KO, Chen Y, Takanohashi A, Spatz M, Hallenbeck JM
Mucosal tolerization to E-selectin protects against memory dysfunction and white matter damage in a vascular cognitive impairment model - J Cereb Blood Flow Metab.   28 341-53 2008

Lee Y, Miyake S, Wakita H, McMullen DC, Azuma Y, Auh S, Hallenbeck JM
Protein SUMOylation is massively increased in hibernation torpor and is critical for the cytoprotection provided by ischemic preconditioning and hypothermia in SH SY 5Y cells - J Cereb Blood Flow Metab   27 950-62 2007

Hallenbeck JM, Hansson GK, Becker KJ.
Immunology of vascular disease: plaque to attack - TRENDS in Immunology   26 550-56 2005



Contact Information

Clinical Investigations Section Stroke Branch, NINDS  Building 10, Room 5B02, MSC 1401  10 Center Drive Bethesda MD  20892-1401

Telephone: 301-496- 6231 (office), 301- 496-6231 (laboratory), 301-402- 2769 (fax), Email: HallenbJ@ninds.nih.gov