法國科學(xué)家日前發(fā)現(xiàn),，早老性癡呆癥的致病蛋白質(zhì)Tau雖然經(jīng)常扮演神經(jīng)細(xì)胞“殺手”的角色，但它在正常情況下卻能對細(xì)胞的DNA（脫氧核糖核酸）進(jìn)行保護(hù),。
這項(xiàng)研究由法國國家科研中心等機(jī)構(gòu)共同完成,。科學(xué)家在美國最新一期《生物化學(xué)雜志》上報(bào)告說,，在患者腦中,，已經(jīng)發(fā)生變異的蛋白質(zhì)Tau會大量吸附磷酸鹽，然后聚集在神經(jīng)細(xì)胞里,，從而引發(fā)早老性癡呆癥,。
不過由呂克·比埃領(lǐng)導(dǎo)的研究小組日前發(fā)現(xiàn)，如果Tau一直處于正常狀態(tài),，沒有吸附過量的磷酸鹽,，那么它就會進(jìn)入神經(jīng)細(xì)胞的細(xì)胞核，對其中的DNA形成保護(hù),?？茖W(xué)家們利用實(shí)驗(yàn)鼠進(jìn)行測試，結(jié)果證實(shí)，在缺乏正常Tau蛋白質(zhì)的情況下,，老鼠腦細(xì)胞中的DNA更易受到損害,。
科學(xué)家表示，這一發(fā)現(xiàn)將幫助科學(xué)家進(jìn)一步了解蛋白質(zhì)Tau的特性,，從而研究出針對早老性癡呆癥的新療法,。
早老性癡呆癥又名阿爾茨海默氏癥，是最常見的老年癡呆癥,，臨床癥狀表現(xiàn)為認(rèn)知,、記憶和語言功能障礙等,。（生物谷Bioon.com）
生物谷推薦原文出處：
JBC doi: 10.1074/jbc.M110.199976
Nuclear tau: a key player in neuronal DNA protection
Audrey Sultan1, Fabrice Nesslany2, Marie Violet1, Severine Begard1, Anne Loyens1, Smail Talahari2, Zeyni Mansuroglu3, Daniel Marzin4, Nicolas Sergeant1, Sandrine Humez1, Morvane Colin1, Eliette Bonnefoy3, Luc Buee1 and Marie-Christine Galas1,*
Abstract
Tau, a neuronal protein involved in neurodegenerative disorders such as Alzheimer disease that is primarily described as a microtubule-associated protein, has also been observed in the nuclei of neuronal and non-neuronal cells. However, the function of the nuclear form of Tau in neurons has not yet been elucidated. In this work, we demonstrate that acute oxidative stress and mild heat stress (HS) induce the accumulation of dephosphorylated Tau in neuronal nuclei. Using chromatin immunoprecipitation assays, we demonstrate that the capacity of endogenous Tau to interact with neuronal DNA increased following HS. Comet assays performed on both wild-type and Tau-deficient neuronal cultures showed that Tau fully protected neuronal genomic DNA against HS-induced damage. Interestingly, HS-induced DNA damage observed in Tau-deficient cells was completely rescued after the over-expression of hTau (human Tau) targeted to the nucleus. These results highlight a novel role for nuclear Tau as a key player in early stress response.
