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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.
Photo of John M. Hallenbeck, M.D., Senior Investigator

Staff:



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.

We also study endogenous neuroprotective mechanisms that induce tolerance to hypoxia and ischemia in brain cells. This work is focused on the intracellular signaling pathways and expressed genes that regulate tolerance to hypoxia and ischemia in hibernating animals (a model of natural tolerance), and in preclinical stroke models and primary cultures of brain microvessel endothelial cells, astrocytes, microglia, cortical neurons and transformed cell lines that have been preconditioned to induce tolerance (models of induced tolerance). Multifunctional regulatory mechanisms that are conserved in the several tolerance models are of particular interest. Findings in preclinical models that have robust potential to treat stroke are carried into proof of concept clinical trials.


Selected Recent Publications:
  • Chen Y Ruetzler C Pandipati S Spatz M McCarron RM Becker K Hallenbeck JM (2003) Mucosal tolerance to E-selectin provides cell-mediated protection against ischemic brain injury. , Proc Natl Acad Sci U S A 100 , 15107-12 . Full Text/Abstract

  • Dirnagl U Simon RP Hallenbeck JM (2003) Ischemic tolerance and endogenous neuroprotection. , Trends Neurosci 26 , 248-54 . Full Text/Abstract

  • Hallenbeck JM (2002) The many faces of tumor necrosis factor in stroke, Nature Medicine 8, 1363-1368. Full Text/Abstract

  • Ginis I, Jaiswal R, Klimanis D, Liu J, Greenspon J, Hallenbeck JM (2002) TNF-alpha-induced tolerance to ischemic injury involves differential control of NFkappaB transactivation: the role of NFkappaB association with p300 adaptor, J Cereb Blood Flow Metab 22, 142-152. Full Text/Abstract

  • Takeda H, Spatz M, Ruetzler C, McCarron R, Becker K, Hallenbeck J (2002) Induction of mucosal tolerance to E-selectin prevents ischemic and hemorrhagic stroke in spontaneously hypertensive genetically stroke-prone rats, Stroke 33, 2156-63. Full Text/Abstract

All Selected Publications


Contact Information:

Dr. John M. Hallenbeck
Clinical Investigations Section
Stroke Branch, NINDS
Building 49, Room 2A10, MSC 4476
49 Convent Drive
Bethesda, MD 20892-4476

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

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Last updated Wednesday, February 01, 2006