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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...

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Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
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Published on: February 16, 2018

Microglia in ischemic brain injury.

Jonathan R Weinstein1, Ines P Koerner, Thomas Möller

  • 1Department of Neurology, School of Medicine, University of Washington, Seattle, Washington 98195-6465, USA Tel.: +1 206 221 5362 jweinste@u.washington.edu.

Future Neurology
|April 20, 2010
PubMed
Summary

Microglia, the brain's immune cells, become activated during cerebral ischemia, contributing to neuroinflammation. Targeting microglial activation shows promise for reducing stroke severity.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglia are key immune cells in the central nervous system (CNS).
  • Cerebral ischemia triggers significant neuroinflammation involving various CNS cells and peripheral immune cells.
  • Microglial activation is a critical response to ischemic conditions.

Purpose of the Study:

  • To review microglial activation in experimental and human ischemia.
  • To present new data on in vitro ischemic effects on microglial phenotype and genomics.
  • To highlight molecular signaling pathways regulating microglial responses.

Main Methods:

  • Literature review of in vitro and in vivo ischemia models.
  • Experimental analysis of microglial phenotype and genomic profiles under ischemic conditions.
  • Review of histological and radiological data in human ischemic stroke.

Main Results:

  • Hypoxia-inducible factor-1 and Toll-like receptor-4 are key regulators of microglial response.
  • Microglial activation is confirmed as a significant factor in human ischemic stroke.
  • In vitro ischemic conditions directly impact microglial phenotype and gene expression.

Conclusions:

  • Microglial activation plays a crucial role in ischemic stroke.
  • Targeting microglia offers potential therapeutic strategies for acute ischemic stroke.
  • Pre-emptive targeting of microglial activation may reduce stroke severity.