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.

Key Words: Cerebral infarction, stroke, kinesin, genetic variant, risk factors