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      Modulators of microglial activation and polarization after intracerebral haemorrhage

      Author(s): , , , ,
      Publication date Created:
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      Journal: Nature Reviews Neurology
      Publisher: Springer Nature

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          Abstract

          Effective drug treatments for intracerebral haemorrhage (ICH) are still lacking. However, therapies that target microglial phenotype switching might soon become available for affected patients. Here, Wang and colleagues summarize key advances in understanding of microglial function after ICH, including modulators of microglial function and interactions with other cells.

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          Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association

          J Claude Hemphill, Steven Greenberg, Craig Anderson … (2015)
          The aim of this guideline is to present current and comprehensive recommendations for the diagnosis and treatment of spontaneous intracerebral hemorrhage.
          Article 0 comments Cited 856 times – based on 0 reviews     Review now
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            The Microglial Sensome Revealed by Direct RNA Sequencing

            Suzanne E Hickman, Nathan D. Kingery, Toshiro K Ohsumi … (2013)
            Microglia, the principal neuroimmune sentinels of the brain, continuously sense changes in their environment and respond to invading pathogens, toxins and cellular debris. Microglia exhibit plasticity and can assume neurotoxic or neuroprotective priming states that determine their responses to danger. We used direct RNA sequencing, without amplification or cDNA synthesis, to determine the quantitative transcriptomes of microglia of healthy adult and aged mice. We validated our findings by fluorescent dual in-situ hybridization, unbiased proteomic analysis and quantitative PCR. We report here that microglia have a distinct transcriptomic signature and express a unique cluster of transcripts encoding proteins for sensing endogenous ligands and microbes that we term the “sensome”. With aging, sensome transcripts for endogenous ligand recognition are downregulated, whereas those involved in microbe recognition and host defense are upregulated. In addition, aging is associated with an overall increase in expression of microglial genes involved in neuroprotection.
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              Microglial and macrophage polarization—new prospects for brain repair.

              Xiaoming Hu, Rehana Leak, Yejie Shi … (2015)
              The traditional view of the adult brain as a static organ has changed in the past three decades, with the emergence of evidence that it remains plastic and has some regenerative capacity after injury. In the injured brain, microglia and macrophages clear cellular debris and orchestrate neuronal restorative processes. However, activation of these cells can also hinder CNS repair and expand tissue damage. Polarization of macrophage populations toward different phenotypes at different stages of injury might account for this dual role. This Perspectives article highlights the specific roles of polarized microglial and macrophage populations in CNS repair after acute injury, and argues that therapeutic approaches targeting cerebral inflammation should shift from broad suppression of microglia and macrophages towards subtle adjustment of the balance between their phenotypes. Breakthroughs in the identification of regulatory molecules that control these phenotypic shifts could ultimately accelerate research towards curing brain disorders.
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                Author and article information

                Journal
                Title: Nature Reviews Neurology
                Abbreviated Title: Nat Rev Neurol
                Publisher: Springer Nature
                ISSN (Print): 1759-4758
                ISSN (Electronic): 1759-4766
                Publication date Created: May 19 2017
                Publication date (Print): May 19 2017
                Volume:
                Issue:
                Article
                DOI: 10.1038/nrneurol.2017.69
                PMC ID: 5575938
                PubMed ID: 28524175
                SO-VID: fed2dc71-1dc4-4bc3-9b1b-8afca4e5d021
                Copyright © © 2017
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