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.