Jiao Bin, Liu Xiaoyan, Zhou Lin, Wang Maggie Haitian, Zhou Yafang, Xiao Tingting, Zhang Weiwei, Sun Rui, Waye Mary Miu Yee, Tang Beisha, Shen Lu
Department of Neurology, Xiangya Hospital, Central South University, Changsha, China.
Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, China.
PLoS One. 2015 Dec 17;10(12):e0144898. doi: 10.1371/journal.pone.0144898. eCollection 2015.
Recently, a number of single nucleotide polymorphisms (SNPs) were identified to be associated with late-onset Alzheimer disease (LOAD) through genome-wide association study data. Identification of SNP-SNP interaction played an important role in better understanding genetic basis of LOAD. In this study, fifty-eight SNPs were screened in a cohort of 229 LOAD cases and 318 controls from mainland China, and their interaction was evaluated by a series of analysis methods. Seven risk SNPs and six protective SNPs were identified to be associated with LOAD. Risk SNPs included rs9331888 (CLU), rs6691117 (CR1), rs4938933 (MS4A), rs9349407 (CD2AP), rs1160985 (TOMM40), rs4945261 (GAB2) and rs5984894 (PCDH11X); Protective SNPs consisted of rs744373 (BIN1), rs1562990 (MS4A), rs597668 (EXOC3L2), rs9271192 (HLA-DRB5/DRB1), rs157581 and rs11556505 (TOMM40). Among positive SNPs presented above, we found the interaction between rs4938933 (risk) and rs1562990 (protective) in MS4A weakened their each effect for LOAD; for three significant SNPs in TOMM40, their cumulative interaction induced the two protective SNPs effects lost and made the risk SNP effect aggravate for LOAD. Finally, we found rs6656401-rs3865444 (CR1-CD33) pairs were significantly associated with decreasing LOAD risk, while rs28834970-rs6656401 (PTK2B-CR1), and rs28834970-rs6656401 (PTK2B-CD33) were associated with increasing LOAD risk. In a word, our study indicates that SNP-SNP interaction existed in the same gene or cross different genes, which could weaken or aggravate their initial single effects for LOAD.
最近,通过全基因组关联研究数据,一些单核苷酸多态性(SNP)被确定与晚发型阿尔茨海默病(LOAD)相关。SNP-SNP相互作用的鉴定在更好地理解LOAD的遗传基础方面发挥了重要作用。在本研究中,对来自中国大陆的229例LOAD病例和318例对照组成的队列进行了58个SNP的筛选,并通过一系列分析方法评估了它们之间的相互作用。确定了7个风险SNP和6个保护性SNP与LOAD相关。风险SNP包括rs9331888(CLU)、rs6691117(CR1)、rs4938933(MS4A)、rs9349407(CD2AP)、rs1160985(TOMM40)、rs4945261(GAB2)和rs5984894(PCDH11X);保护性SNP包括rs744373(BIN1)、rs1562990(MS4A)、rs597668(EXOC3L2)、rs9271192(HLA-DRB5/DRB1)、rs157581和rs11556505(TOMM40)。在上述阳性SNP中,我们发现MS4A基因中的rs4938933(风险)和rs1562990(保护)之间的相互作用削弱了它们各自对LOAD的影响;对于TOMM40中的三个显著SNP,它们的累积相互作用导致两个保护性SNP的作用丧失,并使风险SNP对LOAD的作用加剧。最后,我们发现rs6656401-rs3865444(CR1-CD33)对与降低LOAD风险显著相关,而rs28834970-rs6656401(PTK2B-CR1)和rs28834970-rs6656401(PTK2B-CD33)与增加LOAD风险相关。总之,我们的研究表明,SNP-SNP相互作用存在于同一基因内或跨不同基因,这可能削弱或加剧它们最初对LOAD的单一作用。