猶太大學(xué)醫(yī)學(xué)院的研究人員最近發(fā)現(xiàn)端粒酶過(guò)度活躍以及端粒長(zhǎng)度二者與長(zhǎng)壽有關(guān),。這篇研究報(bào)告發(fā)表在Proceedings of the National Academy of Sciences雜志上。
端粒(Telomeres)是位于染色體末端的一種特殊結(jié)構(gòu),，在衰老,、癌變及其他生物學(xué)過(guò)程中有重要作用，細(xì)胞每分裂一次,，其端粒就相應(yīng)磨損一部分,，當(dāng)端粒變短細(xì)胞停止分裂時(shí)，即進(jìn)入細(xì)胞衰老期(cell senescence),。
課題組的研究人員以德系猶太人（Ashkenazi Jews）為研究對(duì)象,，并將實(shí)驗(yàn)參與者分為三組：第一組86名平均年齡為97歲身體健康的老人,；第二組為175名這些老人的后代；對(duì)照組為93名父母均是正常壽命的子女,。課題組希望通過(guò)該項(xiàng)研究回答兩個(gè)疑問(wèn)：1）壽命較長(zhǎng)的人是不是有更長(zhǎng)的端粒,？ 2）如果是，那么端粒較長(zhǎng)是否與編碼端粒酶的基因發(fā)生變異有關(guān),？通過(guò)研究發(fā)現(xiàn),，上述兩個(gè)問(wèn)題的答案都為“是”。
課題組發(fā)現(xiàn),，壽命更長(zhǎng)的人其端粒的長(zhǎng)度在細(xì)胞分裂過(guò)程中保持得更好,，長(zhǎng)壽的部分原因也可能和細(xì)胞內(nèi)負(fù)責(zé)端粒維持的基因發(fā)生有利變異有關(guān)。
而且,，研究人員發(fā)現(xiàn),，長(zhǎng)壽的老人基因組所攜帶的突變基因能夠使產(chǎn)生端粒酶的系統(tǒng)過(guò)度活躍，從而能夠更高效的維持端粒的長(zhǎng)度,，這些老人中大多數(shù)還能幸免于諸如心血管疾病和糖尿病等老年人常發(fā)生的疾病,。
這項(xiàng)研究表明，端粒長(zhǎng)度以及端粒酶基因變異這兩個(gè)原因?qū)⑹谷祟惖膲勖L(zhǎng),。（生物谷Bioon.com）
端粒是否與長(zhǎng)壽有關(guān),？
端粒研究方興未艾——生物谷專訪童坦君院士和譚錚研究員
衰老機(jī)理研究的“老黃牛”——生物谷專訪印大中教授
端粒及端粒酶研究獲09年諾貝爾生理學(xué)或醫(yī)學(xué)獎(jiǎng)
Nature：研究揭示端粒酶關(guān)鍵部位三維結(jié)構(gòu)
Nat Cell Biol：發(fā)現(xiàn)維持端粒長(zhǎng)度重要分子
PNAS：FOXO3A基因變異的人更加長(zhǎng)壽
Nature：蛔蟲(chóng)的啟示 少食而長(zhǎng)壽
PNAS：蛋白質(zhì)穩(wěn)定性可能是長(zhǎng)壽關(guān)鍵
PNAS：奇特?zé)o毛鼴鼠可能蘊(yùn)藏長(zhǎng)壽秘密
生物谷推薦原始出處：
PNAS November 13, 2009, doi: 10.1073/pnas.0906191106
Genetic variation in human telomerase is associated with telomere length in Ashkenazi centenarians
Gil Atzmonab12, Miook Choa1, Richard M. Cawthonc, Temuri Budagovb, Micol Katzb, Xiaoman Yangb, Glenn Siegelb, Aviv Bergmand, Derek M. Huffmanab, Clyde B. Schechtere, Woodring E. Wrightf, Jerry W. Shayf, Nir Barzilaiab, Diddahally R. Govindarajug and Yousin Suhab2
aDepartments of Medicine and Genetics, Albert Einstein College of Medicine, Bronx, NY 10461
bInstitute for Aging Research, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY 10461
cDepartment of Human Genetics, University of Utah, Salt Lake City, UT 84112
dDepartment of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY 10461
eDepartment of Family and Social Medicine, Albert Einstein College of Medicine, Bronx, NY 10461
fDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390
gDepartment of Neurology, Boston University School of Medicine, Boston, MA 02118
Telomere length in humans is emerging as a biomarker of aging because its shortening is associated with aging-related diseases and early mortality. However, genetic mechanisms responsible for these associations are not known. Here, in a cohort of Ashkenazi Jewish centenarians, their offspring, and offspring-matched controls, we studied the inheritance and maintenance of telomere length and variations in two major genes associated with telomerase enzyme activity, hTERT and hTERC. We demonstrated that centenarians and their offspring maintain longer telomeres compared with controls with advancing age and that longer telomeres are associated with protection from age-related diseases, better cognitive function, and lipid profiles of healthy aging. Sequence analysis of hTERT and hTERC showed overrepresentation of synonymous and intronic mutations among centenarians relative to controls. Moreover, we identified a common hTERT haplotype that is associated with both exceptional longevity and longer telomere length. Thus, variations in human telomerase gene that are associated with better maintenance of telomere length may confer healthy aging and exceptional longevity in humans.
