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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...
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.

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[Gene expression in brain ischemia].

Yoshiki Yagita1, Saburo Sakoda, Kazuo Kitagawa

  • 1Department of Neurology, Osaka University Graduate School of Medicine, 2 2 Yamadaoka, Suita-shi, Osaka 565-0871, Japan.

Brain and Nerve = Shinkei Kenkyu No Shinpo
|December 17, 2008
PubMed
Summary
This summary is machine-generated.

Gene expression changes in the brain during ischemic stress and tolerance offer insights into neuronal survival and recovery. Understanding these gene expression profiles may reveal new therapeutic targets for ischemic stroke.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Context:

  • Ischemic stress triggers dynamic gene expression changes in the brain, including immediate early genes, heat shock proteins, and inflammatory cytokines.
  • Gene expression shifts from neuronal death/survival pathways in the acute phase to neurogenesis and tissue remodeling in the later phase.
  • Ischemic tolerance, a protective mechanism induced by sublethal ischemia, involves altered gene expression patterns.

Purpose:

  • To investigate the role of gene expression in the brain during ischemic stress and the development of ischemic tolerance.
  • To explore how changes in gene expression contribute to neuronal survival, death, and neurological recovery post-ischemia.
  • To identify potential molecular mechanisms underlying ischemic tolerance, focusing on both gene induction and suppression.

Summary:

  • Ischemic stress induces a complex cascade of gene expression in the brain, influencing neuronal fate and tissue repair.
  • Ischemic tolerance is associated with specific gene expression profiles, where both induction (e.g., heat shock proteins) and suppression may play critical roles.
  • Recent studies using gene expression profiling have begun to elucidate the molecular mechanisms of ischemic brain injury and tolerance.

Impact:

  • Gene expression alterations in ischemic stroke provide crucial insights into the brain's response to injury.
  • Understanding the molecular mechanisms of ischemic tolerance could lead to novel therapeutic strategies.
  • Targeting specific gene expression pathways presents a promising avenue for future ischemic stroke treatments.