美國(guó)西北大學(xué)醫(yī)學(xué)院的研究者首次將人類胚胎干細(xì)胞轉(zhuǎn)變一種重要的神經(jīng)元,，它在阿爾茨海默氏?。ɡ夏臧V呆癥）初期死亡,，是記憶喪失的一個(gè)主要原因,。此干細(xì)胞重組和可培育無數(shù)人類神經(jīng)元的技術(shù)，推動(dòng)了治療老年癡呆癥的藥物研發(fā),，研究者能研究神經(jīng)元死亡的原因,，有可能給老年癡呆癥患者移植新的神經(jīng)元。
該研究發(fā)表在3月4日的《干細(xì)胞》雜志上,。這些重要的神經(jīng)元,，被稱為基底前腦膽堿能神經(jīng)元，幫助大腦海馬檢索記憶,。在老年癡呆癥早期,，主要是檢索記憶的能力而非記憶本身丟失了。大腦中的這部分神經(jīng)元數(shù)量相對(duì)較少,，它們的丟失對(duì)于記憶能力會(huì)產(chǎn)生迅速和破壞性的影響,。
西北大學(xué)Feinberg醫(yī)學(xué)院Jack Kessler博士談到，既然我們學(xué)會(huì)了如何生成這些細(xì)胞,，便可以對(duì)其進(jìn)行研究,，并且弄清我們應(yīng)該如何防止其在大腦中死亡。該篇研究的首席作者是Christopher Bissonnette,，該項(xiàng)技術(shù)可以在實(shí)驗(yàn)室里產(chǎn)生大量的神經(jīng)元,，并供其他科學(xué)家對(duì)此進(jìn)行研究。研究者可以迅速測(cè)試數(shù)以千計(jì)的藥物,，這種快速的測(cè)試技術(shù)被稱為高通量篩選技術(shù)(high-throughput screening),。
Kessler 和 Bissonnette將新的神經(jīng)元移植到小鼠的海馬部位，試驗(yàn)表明其運(yùn)作正常,。神經(jīng)元產(chǎn)生軸突,，或?qū)⒗w維與海馬鏈接，釋放乙酰膽堿-大腦海馬需要的化學(xué)物質(zhì),，從而在大腦其他部分檢索記憶,。
人類皮膚細(xì)胞轉(zhuǎn)變成干細(xì)胞及神經(jīng)元
在最新尚未發(fā)表的研究中，西北大學(xué)醫(yī)學(xué)院的科學(xué)家已經(jīng)發(fā)現(xiàn)了制造神經(jīng)元的一種新途徑,。他們從人類皮膚細(xì)胞中獲取人類胚胎干細(xì)胞,，之后將其轉(zhuǎn)化成神經(jīng)元。
科學(xué)家從三類人的皮膚細(xì)胞中提取干細(xì)胞和神經(jīng)元：老年癡呆癥病人,，健康的病人沒有老年癡呆癥家族史，健康的病人但有患老年癡呆癥的可能（由于家族的老年癡呆站病史）,。這對(duì)于研究患病的人類老年癡呆癥細(xì)胞提供了新方法,。
研究者受其患有老年癡呆癥的祖父的影響
由于Bissonnette的祖父死于老年癡呆癥，他一直從事此方面的研究,，他希望使人類干細(xì)胞成為一種健康的替代細(xì)胞,，從而他們能夠?qū)⑵渲踩牖颊叽竽X內(nèi),，以幫助恢復(fù)其功能。Bissonnette必須培育和測(cè)試數(shù)以百萬的細(xì)胞,，從而弄清基因的準(zhǔn)確序列,，從而將干細(xì)胞轉(zhuǎn)化為膽堿能神經(jīng)元。但是僅僅將干細(xì)胞培育成神經(jīng)元還不夠,，Bissonnette要學(xué)會(huì)如何使具有長(zhǎng)久的穩(wěn)定性,，能存活至少20年，以證明他們是可靠的細(xì)胞,。(生物谷Bioon.com)
英文鏈接：http://www.sciencedaily.com/releases/2011/03/110304090455.htm
譯文鏈接：http://www.chinastemcell.org/page/zixun_xwdtlist.aspx?infoid=1010
生物谷推薦英文摘要：
Stem Cells DOI: 10.1002/stem.626
The Controlled Generation of Functional Basal Forebrain Cholinergic Neurons from Human Embryonic Stem Cells
Christopher John Bissonnette1, Ljuba Lyass1, Bula J Bhattacharyya2, Abdelhak Belmadani2, Richard J Miller2, John A Kessler1,*,?
An early substantial loss of basal forebrain cholinergic neurons [BFCN] is a constant feature of Alzheimer's disease and is associated with deficits in spatial learning and memory. The ability to selectively control the differentiation of human embryonic stem cells [hESC] into BFCN would be a significant step towards a cell replacement therapy. We demonstrate here a method for the derivation of a predominantly pure population of BFCN from hESC cells using diffusible ligands present in the forebrain at developmentally relevant time periods. Overexpression of two relevant human transcription factors in hESC-derived neural progenitors also generates BFCN. These neurons express only those markers characteristic of BFCN, generate action potentials, and form functional cholinergic synapses in murine hippocampal slice cultures. siRNA-mediated knockdown of the transcription factors blocks BFCN generation by the diffusible ligands, clearly demonstrating the factors both necessary and sufficient for the controlled derivation of this neuronal population. The ability to selectively control the differentiation of human embryonic stem cells [hESC] into BFCN is a significant step both for understanding mechanisms regulating BFCN lineage commitment and for the development of both cell-transplant-mediated therapeutic interventions for Alzheimer's disease and high throughput screening for agents that promote BFCN survival.
