Evaluation of the Genetic Variants of Kinesin Motor Protein in Ischemic Stroke

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Abstract

Background: The kinesin light-chain 1 genetic variants G56836C, A185C, and C406T were earlier found to amplify the development of leukoaraiosis in hypertensive smokers. These 3 variants were presumed to affect the function of the mitochondria, thereby giving rise to sensitivity to a chronic ischemic state. We have now extended our investigations to examine how the above genetic variants affect the occurrence of ischemic stroke. Methods: Genetic and clinical data on 650 ischemic stroke and 340 neuroimaging alteration-free subjects were analyzed. Univariate and logistic regression approaches were used. Results: None of the above genetic variants proved to be risk factors of ischemic stroke, either alone or in combination with other clinical factors. Conclusion: The examined 3 genetic variants seem to influence the responses of the glial cells to a slight chronic hypoxia state, rather than the mechanisms resulting in cerebral infarcts themselves.

Original languageEnglish
Pages (from-to)360-362
Number of pages3
JournalJournal of Stroke and Cerebrovascular Diseases
Volume18
Issue number5
DOIs
Publication statusPublished - Sep 1 2009

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Keywords

  • Cerebral infarction
  • genetic variant
  • kinesin
  • risk factors
  • stroke

ASJC Scopus subject areas

  • Surgery
  • Rehabilitation
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

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