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Related Concept Videos

Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
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...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...

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TREM2, microglial and ischemic stroke.

Hongxia Wang1, Xiaoling Li1, Qi Wang1

  • 1Department of Neurology, Lanzhou University Second Hospital, Cuiyingmen 82, Chengguan District, Lanzhou, Gansu 730030, China.

Journal of Neuroimmunology
|June 11, 2023
PubMed
Summary
This summary is machine-generated.

This review explores the role of triggering receptor expressed on myeloid cell 2 (TREM2) in ischemic stroke (IS) inflammation and microglia phenotypes. It clarifies TREM2

Keywords:
Immunity and inflammationIschemic strokeMicroglia phenotypeTREM2

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathophysiology

Background:

  • Ischemic stroke (IS) is a major global health concern, with inflammation and immune responses playing critical roles in its development and progression.
  • Microglia, the brain's resident immune cells, exhibit diverse activation states (e.g., M1, M2, DAM, WAMs, SAM) influencing stroke outcomes.
  • The triggering receptor expressed on myeloid cell 2 (TREM2) is implicated in microglial inflammation and phagocytosis post-IS, but its precise link to specific microglial phenotypes remains unclear.

Purpose of the Study:

  • To review and synthesize current knowledge on microglial phenotypic changes and their relationship with inflammatory factors in ischemic stroke.
  • To elucidate the connection between TREM2 receptor expression, inflammatory mediators, and distinct microglial phenotypes following ischemic stroke.
  • To explore TREM2-related signaling pathways, potential therapeutic targets, and the interplay between TREM2, inflammation, and microglia in IS.

Main Methods:

  • Systematic review of existing literature on microglial phenotypes, inflammation, and TREM2 in the context of ischemic stroke.
  • Analysis of transcriptomic data and research on TREM2 expression patterns and their correlation with inflammatory markers.
  • Examination of studies investigating TREM2 signaling pathways and their modulation in experimental stroke models.

Main Results:

  • Microglial activation patterns evolve throughout different pathological stages of ischemic stroke, correlating with specific inflammatory profiles.
  • TREM2 expression is upregulated post-IS and is associated with inflammatory responses and phagocytic activity.
  • While TREM2's role in microglial inflammation and phagocytosis is recognized, its direct relationship with specific complex phenotypes like SAM requires further investigation.

Conclusions:

  • TREM2 plays a significant role in modulating microglial responses, inflammation, and potentially neuroprotection or neurotoxicity after ischemic stroke.
  • Understanding the intricate relationship between TREM2, inflammation, and diverse microglial phenotypes is crucial for developing targeted IS therapies.
  • Further research is needed to fully elucidate the mechanisms involving TREM2 and novel microglia phenotypes, such as stroke-associated microglia (SAM), for potential therapeutic interventions.