近日，倫敦大學(xué)國(guó)王學(xué)院的研究人員與威康信托基金會(huì)桑格研究所合作,，發(fā)現(xiàn)一組“衰老”基因,，這組基因能調(diào)控稱為表觀遺傳因素自然機(jī)制的開啟和閉合，該表觀遺傳因素自然機(jī)制影響老年人的健康和長(zhǎng)壽率,。
這項(xiàng)研究還揭示了由外部因素如飲食,、生活方式和環(huán)境造成的表觀遺傳過程。研究人員說,，他們已經(jīng)確定的表觀遺傳變化可以作為潛在的生物衰老的標(biāo)記物,，并在未來(lái)可能用于抗衰老治療的靶標(biāo)。
相關(guān)研究論文發(fā)表在PLoS Genetics雜志上,，研究人員基于倫敦大學(xué)國(guó)王學(xué)院和圣托馬斯醫(yī)院的數(shù)據(jù)分析研究了172對(duì)32至80歲的雙胞胎,。
研究者對(duì)雙胞胎的DNA表觀遺傳變化進(jìn)行了研究，并進(jìn)行了表觀基因組掃描分析,。他發(fā)現(xiàn)490個(gè)與年齡有關(guān)的表觀遺傳變化,。他們還分析了與年齡相關(guān)的DNA修改，發(fā)現(xiàn)四個(gè)基因的表觀遺傳變化與膽固醇,、肺功能和產(chǎn)婦長(zhǎng)壽等有關(guān),。
研究人員說這些結(jié)果表明,，隨著年齡的增長(zhǎng)，許多與年齡有關(guān)的表觀遺傳變化發(fā)生一個(gè)人的整個(gè)生命中,，這些變化可能在生命的早期階段就開始了,。
Jordana Bell博士來(lái)自倫敦大學(xué)國(guó)王學(xué)院，領(lǐng)導(dǎo)了這項(xiàng)研究,。
我們發(fā)現(xiàn)許多與年齡有關(guān)的表觀遺傳變化,，我們可以運(yùn)用這些研究的結(jié)果成為老齡化的潛在標(biāo)志物。這些結(jié)果可以幫助我們了解老齡人的基本健康情況以及與年齡有關(guān)的疾病的生物學(xué)機(jī)制,。
倫敦大學(xué)國(guó)王學(xué)院Tim Spector教授表示：這項(xiàng)研究首次進(jìn)行大規(guī)模的雙胞胎研究,，并找到的與衰老有關(guān)的關(guān)鍵基因。我們的生活方式可以修改這些基因,，根據(jù)這些基因開發(fā)未來(lái)抗老化療法將是非常激動(dòng)人心的研究,。（生物谷：Bioon.com）
doi:10.1371/journal.pgen.1002629
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Epigenome-Wide Scans Identify Differentially Methylated Regions for Age and Age-Related Phenotypes in a Healthy Ageing Population
Jordana T. Bell, Pei-Chien Tsai, Tsun-Po Yang, Ruth Pidsley, James Nisbet, Daniel Glass, Massimo Mangino,et al.
Age-related changes in DNA methylation have been implicated in cellular senescence and longevity, yet the causes and functional consequences of these variants remain unclear. To elucidate the role of age-related epigenetic changes in healthy ageing and potential longevity, we tested for association between whole-blood DNA methylation patterns in 172 female twins aged 32 to 80 with age and age-related phenotypes. Twin-based DNA methylation levels at 26,690 CpG-sites showed evidence for mean genome-wide heritability of 18%, which was supported by the identification of 1,537 CpG-sites with methylation QTLs in cis at FDR 5%. We performed genome-wide analyses to discover differentially methylated regions (DMRs) for sixteen age-related phenotypes (ap-DMRs) and chronological age (a-DMRs). Epigenome-wide association scans (EWAS) identified age-related phenotype DMRs (ap-DMRs) associated with LDL (STAT5A), lung function (WT1), and maternal longevity (ARL4A, TBX20). In contrast, EWAS for chronological age identified hundreds of predominantly hyper-methylated age DMRs (490 a-DMRs at FDR 5%), of which only one (TBX20) was also associated with an age-related phenotype. Therefore, the majority of age-related changes in DNA methylation are not associated with phenotypic measures of healthy ageing in later life. We replicated a large proportion of a-DMRs in a sample of 44 younger adult MZ twins aged 20 to 61, suggesting that a-DMRs may initiate at an earlier age. We next explored potential genetic and environmental mechanisms underlying a-DMRs and ap-DMRs. Genome-wide overlap across cis-meQTLs, genotype-phenotype associations, and EWAS ap-DMRs identified CpG-sites that had cis-meQTLs with evidence for genotype–phenotype association, where the CpG-site was also an ap-DMR for the same phenotype. Monozygotic twin methylation difference analyses identified one potential environmentally-mediated ap-DMR associated with total cholesterol and LDL (CSMD1). Our results suggest that in a small set of genes DNA methylation may be a candidate mechanism of mediating not only environmental, but also genetic effects on age-related phenotypes.
