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Szolnoki, Z. et al.

Zoltan Szolnoki, Julianna Serly, Andras Kondacs, Yvette Mandi, Ferenc Somogyvari,

Evaluation of the genetic variants of kinesin motor protein in ischemic stroke.

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.[1]

References

Evaluation of the genetic variants of kinesin motor protein in ischemic stroke. Szolnoki, Z., Serly, J., Kondacs, A., Mandi, Y., Somogyvari, F. J. Stroke. Cerebrovasc. Dis (2009) [Pubmed]

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