Please use this identifier to cite or link to this item:
Scopus Web of Science® Altmetric
Type: Journal article
Title: The role of substance P in ischaemic brain injury
Author: Turner, R.
Vink, R.
Citation: Brain Sciences, 2013; 3(1):123-142
Publisher: MDPI
Issue Date: 2013
ISSN: 2076-3425
Statement of
Renée J. Turner and Robert Vink
Abstract: Stroke is a leading cause of death, disability and dementia worldwide. Despite extensive pre-clinical investigation, few therapeutic treatment options are available to patients, meaning that death, severe disability and the requirement for long-term rehabilitation are common outcomes. Cell loss and tissue injury following stroke occurs through a number of diverse secondary injury pathways, whose delayed nature provides an opportunity for pharmacological intervention. Amongst these secondary injury factors, increased blood-brain barrier permeability and cerebral oedema are well-documented complications of cerebral ischaemia, whose severity has been shown to be associated with final outcome. Whilst the mechanisms of increased blood-brain barrier permeability and cerebral oedema are largely unknown, recent evidence suggests that the neuropeptide substance P (SP) plays a central role. The aim of this review is to examine the role of SP in ischaemic stroke and report on the potential utility of NK1 tachykinin receptor antagonists as therapeutic agents.
Keywords: substance P; neuropeptides; neurogenic inflammation; cerebral oedema; stroke; tachykinin; blood-brain barrier; cerebral ischaemia
Rights: © 2013 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (
DOI: 10.3390/brainsci3010123
Grant ID:
Appears in Collections:Aurora harvest 2
Medical Sciences publications

Files in This Item:
File Description SizeFormat 
hdl_90145.pdfPublished version1.66 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.