Targeting Microglial Activation in Stroke Therapy: Pharmacological Tools and Gender Effects

ISSN: 1875-533X (Online)
ISSN: 0929-8673 (Print)

Volume 24, 42 Issues, 2017

Download PDF Flyer

Current Medicinal Chemistry

This journal supports open access

Aims & ScopeAbstracted/Indexed in

Ranking and Category:
  • 10th of 59 in Chemistry & Medicinal
  • 63rd of 253 in Pharmacology & Pharmacy
  • 100th of 289 in Biochemistry & Molecular Biology

Submit Abstracts Online Submit Manuscripts Online

Atta-ur-Rahman, FRS
Honorary Life Fellow
Kings College
University of Cambridge

View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Current: 3.455
5 - Year: 3.792

Targeting Microglial Activation in Stroke Therapy: Pharmacological Tools and Gender Effects

Current Medicinal Chemistry, 21(19): 2146-2155.

Author(s): Y. Chen, S.J. Won, Y. Xu and RA Swanson.

Affiliation: Dept. of Neurology, University of California San Francisco; and Neurology Service, San Francisco Veterans Affairs Medical Center, 4150 Clement St, San Francisco, CA 94121, USA.


Ischemic stroke is caused by critical reductions in blood flow to brain or spinal cord. Microglia are the resident immune cells of the central nervous system, and they respond to stroke by assuming an activated phenotype that releases cytotoxic cytokines, reactive oxygen species, proteases, and other factors. This acute, innate immune response may be teleologically adapted to limit infection, but in stroke this response can exacerbate injury by further damaging or killing nearby neurons and other cell types, and by recruiting infiltration of circulating cytotoxic immune cells. The microglial response requires hours to days to fully develop, and this time interval presents a clinically accessible time window for initiating therapy. Because of redundancy in cytotoxic microglial responses, the most effective therapeutic approach may be to target the global gene expression changes involved in microglial activation. Several classes of drugs can do this, including histone deacetylase inhibitors, minocycline and other PARP inhibitors, corticosteroids, and inhibitors of TNFα and scavenger receptor signaling. Here we review the pre-clinical studies in which these drugs have been used to suppress microglial activation after stroke. We also review recent advances in the understanding of sex differences in the CNS inflammatory response, as these differences are likely to influence the efficacy of drugs targeting post-stroke brain inflammation.


Brain, corticosteroid, female, HDAC, inflammation, ischemia, minocycline, PARP.

Purchase Online Order Reprints Order Eprints Rights and Permissions

Article Details

Volume: 21
Issue Number: 19
First Page: 2146
Last Page: 2155
Page Count: 10
DOI: 10.2174/0929867321666131228203906
Price: $58
Global Biotechnology Congress 2017Drug Discovery and Therapy World Congress 2017Drug Discovery 2017

Related Journals

Related eBooks

Webmaster Contact: Copyright © 2017 Bentham Science