Gene–environmental effects behind leukoaraiosis: a silent genetic variant of the kinesin protein can be activated in a subject with poorly controlled long-lasting hypertension

• Published in: Clinical biochemistry Vol. 42; no. 7; pp. 630 - 633
• Main Authors: Szolnoki, Zoltan, Kondacs, Andras, Mandi, Yvette, Somogyvari, Ferenc
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2009
• Subjects: Aged; Attention; Female; Gene; Genetic Predisposition to Disease; Genetic variant; Gene–environmental interaction; Genotype; Humans; Hypertension - complications; Hypertension - genetics; Kinesin; Kinesin - genetics; Leukoaraiosis; Leukoaraiosis - genetics; Leukoaraiosis - pathology; Male; Middle Aged; White matter damage; White matter damage; Gene; Leukoaraiosis; Genetic variant; Gene–environmental interaction; Kinesin
• ISSN: 0009-9120; 1873-2933
• DOI: 10.1016/j.clinbiochem.2008.11.003

The rs8702 variant of the kinesin light chain 1 was earlier found to be a risk factor for vascular white matter demyelinization, referred to as leukoaraiosis (LA), in hypertensive smokers. The aim of this study was to determine the extent to which this genetic variant gives rise to the occurrence of LA and its severity, if the subject is exposed to long-lasting, severe and poorly controlled hypertension. The clinical and genetic data on 204 LA patients without infarction and 240 neuroimaging alteration-free subjects were analyzed. The rs8702 CC genotype proved to exert strong amplifying effects on the occurrence and severity of LA in patients with long-lasting poorly controlled severe hypertension (a 25.9-fold risk of LA in carriers relative to non-carriers; p < 0.001). The previous data on hypertensive smokers and the present findings suggest that the rs8702 CC variant is increasingly unfavorable as regards LA if the hypertension is more severe and poorly controlled. This draws attention to a need for stricter preventive measures in CC carriers.