期刊文献+

细胞间黏附分子-1基因多态性与老年无症状性脑白质损害的相关性 被引量:3

Association between intercellular adhesion molecule-1 K469E polymorphism and white matter lesions in asymptomatic elderly people
原文传递
导出
摘要 目的 探讨健康老年人无症状性脑白质损害(WML)和细胞间黏附分子1 (ICAM -1)K469E基因多态性之间的关系。方法 利用聚合酶链式反应限制性片段长度多态性法(PCR RFLP),对121例WML患者和99名对照组老年人的ICAM 1K469E基因多态性位点进行检测和分析。结果 病例组和对照组ICAM 1K469E多态性分布符合Hardy Weinberg遗传平衡定律,说明研究对象具有群体代表性。WML组KK基因型和K等位基因频率均明显高于对照组(基因型50. 4%vs25. 3%,P<0. 01;等位基因频率73 .1% vs52. 0%,P=0 .002),两组间差异有统计学意义。Logistic多因素回归分析显示在校正高血压、年龄等因素后,ICAM 1KK型与WML的发生相关(OR=2 99,P=0. 01)。和非KK型个体相比,KK型个体患WML相对危险度是前者的2. 99倍。结论 ICAM 1KK基因型与WML的发生具有相关性,提示ICAM 1基因K469E多态性可能是中国人WML发病的遗传学危险因素。 Objective To evaluate the relationship between intercellular adhesion molecule-1 (ICAM-1) gene K469E polymorphism and white matter lesions (WML) in asymptomatic elderly people.Methods One hundred and twenty-one patients with WML and ninety-nine controls were included in the study. ICAM-1 genotypes were evaluated by polymerse chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Results Distributions of each genotype in patient and control groups were in agreement with Hardy-Weinberg equilibrium, indicating that no apparent bias was observed in the populations. The frequency of ICAM-1 KK genotype and K allele were higher in patients with WML than in those without (genotype 50.4% vs 25.3%,P<0.01; allele 73.1% vs 52.0%, P=0.002), the differences between the two groups were significant. In the multiple logistic regression analysis, independent of other risk factors such as hypertension and age, the ICAM-1 KK genotype was associated with a 2.99-fold increased risk for WML.Conclusions We found a significant association between the KK genotype and the presence of WML, these data suggest that the ICAM-1 K469E polymorphism could be a genetic risk factors for WML in asymptomatic elderly people.
出处 《中华神经科杂志》 CAS CSCD 北大核心 2005年第4期247-250,共4页 Chinese Journal of Neurology
  • 相关文献

参考文献10

  • 1Pantoni L, Simoni M, Pracucci G, et al. Visual rating scales for age-related white matter changes ( leukoaraiosis ) : can the heterogeneity be reduced? Stroke, 2002, 33:2827-2833.
  • 2Pantoni L, Garcia JH. The significance of cerebral white matter abnormalities 100 years after Binswanger's report. Stroke, 1995,26:1293-1301.
  • 3Carmelli R, Decarli C, Swan G, et al. Evidence for genetic variance in white matter hyperintensity volume in normal elderly male twins.Stroke, 1998, 29: 1177-1181.
  • 4Kamiuchi K, Hasegawa G, Obayashi H, et al. Intercellular adhesion molecule-1 (ICAM-1) polymorphism is associated with diabetic retinopathy in Type 2 diabetes mellitus. Diabet Med, 2002, 19:371 -376.
  • 5Pola R, Flex A, Gaetani E, et al. Synergistic effect of - 174 G/C polymorphism of the interleukin-6 gene promoter and 469 E/K polymorphism of the intercellular adhesion molecule-1 gene in Italian patients with history of ischemic stroke. Stroke, 2003, 34:881-885.
  • 6Pola R, Flex A, Gaetani E, et al. Association between intercellular adhesion molecule-1 E/K gene polymorphism and probable vascular dementia in humans. Neumsci Let, 2002, 326: 171-174.
  • 7Fazekas F, Kleinert R, Offenbacher H, et al. Pathologic correlates of incidental MRI white matter signal hyperintensities. Neurology,1993,43 : 1683-1689.
  • 8Breteler MM, van Swieten JC, Bots ML, et al. Cerebral white matter lesions, vascular risk factors, and cognitive function in a populationbased study: the Rotterdam Study. Neurology, 1994, 44: 1246-1252.
  • 9Cybulsky MI, Gimbrone MA. Endothelial expression of amononuclear leukocyte adhesion molecule during atherogenesis.Science, 1991, 251 : 788-791.
  • 10Staunton DE, Dustin ML, Erickson HP, et al. The arrangement of the immunoglobulin-like domains of ICAM-1 and the binding sites for LFA-1 and rhinovirus. Cell, 1990, 61:243-254.

同被引文献11

引证文献3

二级引证文献11

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部