4个长寿基因被发现:与血型、阿尔兹海默症等疾病相关联
2015/12/22
近期,桑福德大学发育生物学和遗传学教授Stuart Kim带领的研究团队发表文章证实,找到4个与长寿相关联的特殊基因:ABO基因,参与决定血型;CDKN2B基因,调控细胞分裂;APOE基因,与阿尔兹海默症相关;SH2B3基因,曾被证实与延长果蝇寿命有关。


近期,桑福德大学发育生物学和遗传学教授Stuart Kim带领的研究团队发表文章证实,找到4个与长寿相关联的特殊基因:ABO基因,参与决定血型;CDKN2B基因,调控细胞分裂;APOE基因,与阿尔兹海默症相关;SH2B3基因,曾被证实与延长果蝇寿命有关。

桑福德大学发育生物学和遗传学教授Stuart Kim 表示,百岁老人之所以长寿肯定与基因有关系。他们研究的初衷就是找到其中的联系,揭开为什么有些人比一般人长寿的谜底。相关研究成果于12月17日发表在《PLOS Genetics》期刊。研究人员表示希望以此为基础,挖掘到更多有长寿相关联的基因,并深入研究这些关键基因影响衰老的路径。

长寿基因:与血型、细胞分裂以及阿尔兹海默症等疾病相关

过去围绕长寿的研究基本都是通过比较老年群体和年轻群体,筛查差异基因。但是这样的研究方法可能会错过一些重要的关联。

不同于以往的研究策略,Kim研究团队缩小基因筛查范围,只关注那些已知的与影响生命长短的疾病有关系的基因,例如心脏病和阿尔兹海默症。因为这些疾病会增加患者早逝的风险,而且与疾病相关的基因突变会增加患病的概率,从而减少长寿的可能。

以800个100岁以上、5400个90岁以上的老人为筛查对象,研究人员找到8个与长寿相关的基因。再针对1000个百岁老人进行分析后,最终确定了4个关键基因——ABO、CDKN2B、 APOE和SH2B3。

研究发现相比于普通人,这4个关键基因在百岁老人的基因组中更为普遍。

例如,参与调查的百岁老人中,表现为O型血的较多。ABO基因决定的O型血的老年人相比于其他血型的人,患冠状动脉心脏病和癌症的风险相对较低,且胆固醇水平较低。CDKN2B基因与细胞分裂有关,决定细胞是否继续分裂或者停止分裂。Kim认为,减缓细胞衰老可能是一个有助于长寿的策略。

Kim表示,与长寿相关的基因还有很多。他希望,这4个关键基因的挖掘能够为其他研究做铺垫,以筛查出更多与寿命、抗衰老相关的基因。

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  • Genome-Wide Scan Informed by Age-Related Disease Identifies Loci for Exceptional Human Longevity

    We developed a new statistical framework to find genetic variants associated with extreme longevity. The method, informed GWAS (iGWAS), takes advantage of knowledge from large studies of age-related disease in order to narrow the search for SNPs associated with longevity. To gain support for our approach, we first show there is an overlap between loci involved in disease and loci associated with extreme longevity. These results indicate that several disease variants may be depleted in centenarians versus the general population. Next, we used iGWAS to harness information from 14 meta-analyses of disease and trait GWAS to identify longevity loci in two studies of long-lived humans. In a standard GWAS analysis, only one locus in these studies is significant (APOE/TOMM40) when controlling the false discovery rate (FDR) at 10%. With iGWAS, we identify eight genetic loci to associate significantly with exceptional human longevity at FDR < 10%. We followed up the eight lead SNPs in independent cohorts, and found replication evidence of four loci and suggestive evidence for one more with exceptional longevity. The loci that replicated (FDR < 5%) included APOE/TOMM40 (associated with Alzheimer’s disease), CDKN2B/ANRIL (implicated in the regulation of cellular senescence), ABO (tags the O blood group), and SH2B3/ATXN2 (a signaling gene that extends lifespan in Drosophila and a gene involved in neurological disease). Our results implicate new loci in longevity and reveal a genetic overlap between longevity and age-related diseases and traits, including coronary artery disease and Alzheimer’s disease. iGWAS provides a new analytical strategy for uncovering SNPs that influence extreme longevity, and can be applied more broadly to boost power in other studies of complex phenotypes.

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