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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...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
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.
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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Correlation between cerebral infarction and ALOX5AP gene expression.

Chen Xu1, Li Qiang, Cao Limei

  • 1Department of Neurology, The Eighth Shanghai People Hospital, Affiliated to Jiangsu University, Shangai, 200235, China, cxwp65@163.com.

Cell Biochemistry and Biophysics
|April 3, 2013
PubMed
Summary

The Arachidonate 5-lipoxygenase activating protein (ALOX5AP) gene was investigated as a risk factor for cerebral infarction in the Chinese Han population. Genetic analysis revealed no association between ALOX5AP polymorphisms (SG13S114, SG13S32) and cerebral infarction risk.

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Area of Science:

  • Genetics
  • Neurology
  • Epidemiology

Background:

  • Previous studies suggested the ALOX5AP gene as a potential risk factor for cerebral infarction.
  • Verification of this association in diverse populations, such as the Chinese Han population, is crucial.

Purpose of the Study:

  • To investigate the association between ALOX5AP gene polymorphisms and cerebral infarction in the Chinese Han population.
  • To determine if specific single-nucleotide polymorphisms (SNPs) in ALOX5AP confer risk for cerebral infarction.

Main Methods:

  • Case-control study involving 547 cerebral infarction patients and 794 healthy controls.
  • Genotyping of four ALOX5AP SNPs (SG13S25, SG13S114, SG13S89, SG13S32) using real-time quantitative PCR and allele-specific PCR.
  • Linkage disequilibrium analysis was performed.

Main Results:

  • Allelic frequencies for SG13S114 and SG13S32 were above 5%, while SG13S25 and SG13S89 were below 5%.
  • No significant differences were observed in allele, genotype, or haplotype frequencies between cerebral infarction cases and controls for the studied SNPs.
  • The ALOX5AP gene polymorphisms SG13S114 and SG13S32 showed no association with cerebral infarction in this population.

Conclusions:

  • The investigated ALOX5AP gene polymorphisms (SG13S114 and SG13S32) are not associated with cerebral infarction in the Chinese Han population.
  • These findings suggest that ALOX5AP may not be a significant genetic risk factor for cerebral infarction in this specific ethnic group.