Kim Sungeun, Nho Kwangsik, Ramanan Vijay K, Lai Dongbing, Foroud Tatiana M, Lane Katie, Murrell Jill R, Gao Sujuan, Hall Kathleen S, Unverzagt Frederick W, Baiyewu Olusegun, Ogunniyi Adesola, Gureje Oye, Kling Mitchel A, Doraiswamy P Murali, Kaddurah-Daouk Rima, Hendrie Hugh C, Saykin Andrew J
Center for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN, USA.
Indiana Alzheimer Disease Center, Indiana University School of Medicine, Indianapolis, IN, USA.
J Alzheimers Dis. 2016;49(4):991-1003. doi: 10.3233/JAD-150651.
Plasma homocysteine, a metabolite involved in key cellular methylation processes seems to be implicated in cognitive functions and cardiovascular health with its high levels representing a potential modifiable risk factor for Alzheimer's disease (AD) and other dementias. A better understanding of the genetic factors regulating homocysteine levels, particularly in non-white populations, may help in risk stratification analyses of existing clinical trials and may point to novel targets for homocysteine-lowering therapy. To identify genetic influences on plasma homocysteine levels in individuals with African ancestry, we performed a targeted gene and pathway-based analysis using a priori biological information and then to identify new association performed a genome-wide association study. All analyses used combined data from the African American and Yoruba cohorts from the Indianapolis-Ibadan Dementia Project. Targeted analyses demonstrated significant associations of homocysteine and variants within the CBS (Cystathionine beta-Synthase) gene. We identified a novel genome-wide significant association of the AD risk gene CD2AP (CD2-associated protein) with plasma homocysteine levels in both cohorts. Minor allele (T) carriers of identified CD2AP variant (rs6940729) exhibited decreased homocysteine level. Pathway enrichment analysis identified several interesting pathways including the GABA receptor activation pathway. This is noteworthy given the known antagonistic effect of homocysteine on GABA receptors. These findings identify several new targets warranting further investigation in relation to the role of homocysteine in neurodegeneration.
血浆同型半胱氨酸是一种参与关键细胞甲基化过程的代谢产物,似乎与认知功能和心血管健康有关,其高水平代表了阿尔茨海默病(AD)和其他痴呆症潜在的可改变风险因素。更好地了解调节同型半胱氨酸水平的遗传因素,特别是在非白人人群中,可能有助于现有临床试验的风险分层分析,并可能指向降低同型半胱氨酸治疗的新靶点。为了确定非洲裔个体血浆同型半胱氨酸水平的遗传影响,我们使用先验生物学信息进行了靶向基因和基于通路的分析,然后进行全基因组关联研究以确定新的关联。所有分析都使用了来自印第安纳波利斯 - 伊巴丹痴呆项目的非裔美国人和约鲁巴队列的合并数据。靶向分析表明同型半胱氨酸与CBS(胱硫醚β合酶)基因内的变异存在显著关联。我们在两个队列中均发现AD风险基因CD2AP(CD2相关蛋白)与血浆同型半胱氨酸水平存在全基因组显著关联。已鉴定的CD2AP变异(rs6940729)的次要等位基因(T)携带者的同型半胱氨酸水平降低。通路富集分析确定了几个有趣的通路,包括GABA受体激活通路。鉴于同型半胱氨酸对GABA受体已知的拮抗作用,这一点值得注意。这些发现确定了几个新的靶点,值得进一步研究同型半胱氨酸在神经退行性变中的作用。