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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.
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...
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...
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...
Ischemic Heart Disease: Overview01:17

Ischemic Heart Disease: Overview

Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...

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High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
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Glycoprotein Ib-alpha Kozak polymorphism in ischemic stroke.

Fatma Inci Esen1, Veysel Sabri Hancer, Reyhan Diz Küçükkaya

  • 1Edip Aktin Stroke Unit, Istanbul Medical Faculty, Istanbul University, Turkey. fesseden@superposta.com

Neurological Research
|December 27, 2011
PubMed
Summary

The glycoprotein Ib-alpha (GPIb-alpha) T/C polymorphism may increase ischemic stroke risk. This genetic variation, particularly the -5C allele, was more prevalent in stroke patients, especially those with undetermined causes.

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Area of Science:

  • Genetics
  • Cardiovascular Medicine
  • Neurology

Background:

  • A T/C polymorphism in the Kozak sequence of the glycoprotein Ib-alpha (GPIb-alpha) gene at position -5 has been identified.
  • The -5C allele is associated with increased surface expression of the GPIb-IX-V complex.
  • Elevated GPIb-IX-V complex levels may enhance platelet adhesion and increase thrombosis risk.

Purpose of the Study:

  • To investigate the association between the GPIb-alpha Kozak polymorphism and ischemic stroke risk.

Main Methods:

  • A prospective study involving 231 first-ever ischemic stroke patients and 220 healthy controls.
  • Analysis of demographic features, risk factors, clinical presentation, and etiological subtypes.
  • Genotyping for the GPIb-alpha T/C polymorphism.

Main Results:

  • Carriers of at least one C allele were significantly overrepresented in the ischemic stroke group (32.5%) compared to controls (23%) (OR: 0.61; P = 0.03).
  • The C allele distribution was highest in stroke patients with undetermined etiology (45%), significantly exceeding controls (OR: 0.36; P = 0.0008).
  • No significant association was found in other etiological subtypes.

Conclusions:

  • The GPIb-alpha T/C polymorphism, specifically the -5C allele, may be a risk factor for ischemic stroke.
  • This association appears particularly relevant in ischemic stroke cases with undetermined etiology.