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

Research output: Article

3 Citations (Scopus)

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 - szept. 2009

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Kinesin
Stroke
Leukoaraiosis
Proteins
Neuroimaging
Neuroglia
Mitochondria
Logistic Models
Light

ASJC Scopus subject areas

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

Cite this

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title = "Evaluation of the Genetic Variants of Kinesin Motor Protein in Ischemic Stroke",
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.",
keywords = "Cerebral infarction, genetic variant, kinesin, risk factors, stroke",
author = "Z. Szolnoki and Julianna Serly and A. Kondacs and Y. M{\'a}ndi and F. Somogyv{\'a}ri",
year = "2009",
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doi = "10.1016/j.jstrokecerebrovasdis.2009.01.004",
language = "English",
volume = "18",
pages = "360--362",
journal = "Journal of Stroke and Cerebrovascular Diseases",
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publisher = "W.B. Saunders Ltd",
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TY - JOUR

T1 - Evaluation of the Genetic Variants of Kinesin Motor Protein in Ischemic Stroke

AU - Szolnoki, Z.

AU - Serly, Julianna

AU - Kondacs, A.

AU - Mándi, Y.

AU - Somogyvári, F.

PY - 2009/9

Y1 - 2009/9

N2 - 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.

AB - 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.

KW - Cerebral infarction

KW - genetic variant

KW - kinesin

KW - risk factors

KW - stroke

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