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Blocking Neurogenic Inflammation for the Treatment of Acute Disorders of the Central Nervous System
Author(s) -
Kate Lewis,
Renée J. Turner,
Robert Vink
Publication year - 2013
Publication title -
international journal of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.106
H-Index - 33
eISSN - 2090-8040
pISSN - 2042-0099
DOI - 10.1155/2013/578480
Subject(s) - medicine , neurogenic inflammation , inflammation , central nervous system , substance p , pathogenesis , microglia , blood–brain barrier , nervous system , spinal cord injury , traumatic brain injury , neuroscience , receptor , spinal cord , immunology , neuropeptide , biology , psychiatry
Classical inflammation is a well-characterized secondary response to many acute disorders of the central nervous system. However, in recent years, the role of neurogenic inflammation in the pathogenesis of neurological diseases has gained increasing attention, with a particular focus on its effects on modulation of the blood-brain barrier BBB. The neuropeptide substance P has been shown to increase blood-brain barrier permeability following acute injury to the brain and is associated with marked cerebral edema. Its release has also been shown to modulate classical inflammation. Accordingly, blocking substance P NK1 receptors may provide a novel alternative treatment to ameliorate the deleterious effects of neurogenic inflammation in the central nervous system. The purpose of this paper is to provide an overview of the role of substance P and neurogenic inflammation in acute injury to the central nervous system following traumatic brain injury, spinal cord injury, stroke, and meningitis.

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