Description of Invention: Available for licensing are methods and formulations for treating or preventing Vascular Cognitive Impairment (VCI) through mucosal administration of E-selectin, an inducible adhesion molecule on endothelial cells. Vascular dementia is defined as the loss of cognitive function resulting from ischemic, ischemic-hypoxic, or hemorrhagic brain lesions as a result of cerebrovascular diseases and pathologic changes. Presently no adequate medical treatment exists for VCI.
Cerebrovascular disease causes proinflammatory cytokines such as IL-1 and TNF to induce the expression of E-selectin on human endothelium. E-selectin mediates the adhesion of various leukocytes, including neutrophils, monocytes, eosinophils, natural killer cells, and a subset of T cells to the activated endothelium. Activation of vascular endothelial cells by proinflammatory cytokines is believed to be involved in conversion of the luminal surface of endothelium from anticoagulant and anti-inflammatory to procoagulant and pro-inflammatory. These vascular changes are thought to underlie the development of VCI.
Mucosally administered antigens can inhibit immune responses in an antigen specific fashion by inducing a subset of lymphocytes to produce anti-inflammatory cytokines in the presence of the antigen. This type of tolerance has been termed "bystander suppression". In an animal model of VCI, intranasal administered E-selectin suppressed activation of vessel segments beginning to express E-selectin and thus prevented the development of VCI. Immunosuppression via antigen-specific modulation of the immune response (mucosal tolerance) should have no systemic immunosuppressive effects.
Inventors: John M Hallenbeck (NINDS)
Patent Status: HHS, Reference No. E-271-2005/0
Licensing Status: Available for non-exclusive or exclusive licensing.
Collaborative Research Opportunity: The NINDS Stroke Branch is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize the use of E-selectin for treatment of VCI. For more information, please contact: Laurie Arrants, NINDS Technology Transfer Office, 301-435-3112; arrantsl@ninds.nih.gov.
Portfolios: Central Nervous System Central Nervous System - Therapeutics
For Additional Information Please Contact: Norbert Pontzer Ph.D., J.D. NIH Office of Technology Transfer 6011 Executive Blvd. Suite 325
Room 23, Rockville, MD 20852 United States Email: pontzern@mail.nih.gov Phone: 301-435-5502 Fax: 301-402-0220
Description of Invention:
Available for licensing are methods and formulations for treating or preventing Vascular Cognitive Impairment (VCI) through mucosal administration of E-selectin, an inducible adhesion molecule on endothelial cells. Vascular dementia is defined as the loss of cognitive function resulting from ischemic, ischemic-hypoxic, or hemorrhagic brain lesions as a result of cerebrovascular diseases and pathologic changes. Presently no adequate medical treatment exists for VCI.
Cerebrovascular disease causes proinflammatory cytokines such as IL-1 and TNF to induce the expression of E-selectin on human endothelium. E-selectin mediates the adhesion of various leukocytes, including neutrophils, monocytes, eosinophils, natural killer cells, and a subset of T cells to the activated endothelium. Activation of vascular endothelial cells by proinflammatory cytokines is believed to be involved in conversion of the luminal surface of endothelium from anticoagulant and anti-inflammatory to procoagulant and pro-inflammatory. These vascular changes are thought to underlie the development of VCI.
Mucosally administered antigens can inhibit immune responses in an antigen specific fashion by inducing a subset of lymphocytes to produce anti-inflammatory cytokines in the presence of the antigen. This type of tolerance has been termed "bystander suppression". In an animal model of VCI, intranasal administered E-selectin suppressed activation of vessel segments beginning to express E-selectin and thus prevented the development of VCI. Immunosuppression via antigen-specific modulation of the immune response (mucosal tolerance) should have no systemic immunosuppressive effects.
Inventors:
John M Hallenbeck (NINDS)
Patent Status:
HHS, Reference No. E-271-2005/0
Licensing Status:
Available for non-exclusive or exclusive licensing.
Collaborative Research Opportunity:
The NINDS Stroke Branch is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize the use of E-selectin for treatment of VCI. For more information, please contact: Laurie Arrants, NINDS Technology Transfer Office, 301-435-3112; arrantsl@ninds.nih.gov.
Portfolios:
Central Nervous System
Central Nervous System - Therapeutics
For Additional Information Please Contact:
Norbert Pontzer Ph.D., J.D.
NIH Office of Technology Transfer
6011 Executive Blvd. Suite 325 Room 23,
Rockville, MD 20852
United States
Email: pontzern@mail.nih.gov
Phone: 301-435-5502
Fax: 301-402-0220
Ref No: 1447
Updated: 09/2006