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Updated: Jun 1, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Genetic susceptibility to ischemic stroke.

James F Meschia¹, Bradford B Worrall, Stephen S Rich

¹Department of Neurology, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224, USA. meschia.james@mayo.edu

Nature Reviews. Neurology

|June 2, 2011

Summary

This summary is machine-generated.

Genetic factors in ischemic stroke are complex. While single-gene disorders like sickle cell disease are important, common genetic variants have minor effects. Research is ongoing to understand stroke genetics and its clinical application.

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Published on: May 9, 2013

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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

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Published on: August 18, 2015

Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia

Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia

Published on: May 9, 2013

Area of Science:

Neurology
Genetics
Internal Medicine

Background:

Ischemic stroke has several associated single-gene disorders.
Genome-wide association studies (GWAS) have not identified major common genetic risk variants for ischemic stroke.
Pharmacogenomic studies have identified genetic factors influencing response to stroke medications.

Purpose of the Study:

To review single-gene disorders associated with ischemic stroke.
To summarize current research on genetic risk factors for ischemic stroke.
To discuss the role of pharmacogenomics in stroke treatment.

Main Methods:

Literature review of single-gene disorders and ischemic stroke.
Summary of findings from candidate gene and genome-wide association studies.
Discussion of pharmacogenomic data relevant to stroke.

Main Results:

Several single-gene disorders present with ischemic stroke.
No single common genetic variant has been found to significantly increase ischemic stroke risk.
Ongoing large-scale studies aim to identify common variants with smaller effects.
Genetic factors influencing response to warfarin, statins, and clopidogrel have been identified.

Conclusions:

Awareness of single-gene disorders is crucial for clinicians treating stroke patients.
Current understanding of common genetic variants offers limited major risk prediction.
Integrating genetic knowledge into clinical practice for stroke remains a challenge.
Pharmacogenomics offers potential for personalized stroke treatment.