研究人員發(fā)現(xiàn)了一種有助于大腦長出新細(xì)胞的藥物,，并稱他們的研究可能有助于提高治療老年癡呆癥試驗藥物的療效,。
此前已有研究表明，包括人類在內(nèi),，所有哺乳動物在整個生命周期都會制造腦細(xì)胞,。其中多數(shù)新生腦細(xì)胞都會死亡，但最新研究發(fā)現(xiàn)的藥物能幫助更多的新生細(xì)胞存活,，并成長為真正活躍的腦細(xì)胞,。
>>>借著上海世博會的良好契機(jī)，"第一屆腫瘤基礎(chǔ)和轉(zhuǎn)化醫(yī)學(xué)國際研討會"將于2010年10月12日在中國上海盛大開幕,，這將為廣大活躍在腫瘤基礎(chǔ)和轉(zhuǎn)化醫(yī)學(xué)第一線的科研工作者提供一個互動交流的平臺,。
會議官方網(wǎng)站：www.cancerasia.org
得克薩斯大學(xué)西南醫(yī)療中心的Andrew Pieper在電話采訪中表示：“我們的大腦每天都在產(chǎn)生新的神經(jīng)元。新發(fā)現(xiàn)的藥物能允許更多神經(jīng)元存活,。”
這種藥物暫時命名為P7C3,，研究人員已著手提高其療效。他們稱這種藥物似乎很安全,，即使作為藥丸服下也可起效,。
Pieper和同事們在《細(xì)胞》(Cell)雜志發(fā)表報告稱，這種藥物類似于Medivation公司和輝瑞公司聯(lián)合開發(fā)的老年癡呆癥試驗性藥物Dimebon,，且可能有助于改善其藥效,。(生物谷Bioon.net)
更多閱讀
澳大利亞科學(xué)家發(fā)現(xiàn)腦細(xì)胞老化原因
J. Neurosci：腦細(xì)胞可再生形成神經(jīng)細(xì)胞
Nature：Notch蛋白可修復(fù)腦細(xì)胞
Nat. Neuro.：培養(yǎng)皿中的腦細(xì)胞網(wǎng)絡(luò)有計時功能
Nature Neurosci: 研究發(fā)現(xiàn)大腦細(xì)胞的全新工作機(jī)制
生物谷推薦原文出處：
Cell doi：10.1016/j.cell.2010.06.018
Discovery of a Proneurogenic, Neuroprotective Chemical
Andrew A. Pieper, Shanhai Xie, Emanuela Capota, Sandi Jo Estill, Jeannie Zhong, Jeffrey M. Long, Ginger L. Becker, Paula Huntington, Shauna E. Goldman, Ching-Han Shen, Maria Capota, Jeremiah K. Britt, Tiina Kotti, Kerstin Ure, Daniel J. Brat, Noelle S. Williams, Karen S. MacMillan, Jacinth Naidoo, Lisa Melito, Jenny Hsieh, Jef De Brabander, Joseph M. Ready, Steven L. McKnight
An in vivo screen was performed in search of chemicals capable of enhancing neuron formation in the hippocampus of adult mice. Eight of 1000 small molecules tested enhanced neuron formation in the subgranular zone of the dentate gyrus. Among these was an aminopropyl carbazole, designated P7C3, endowed with favorable pharmacological properties. In vivo studies gave evidence that P7C3 exerts its proneurogenic activity by protecting newborn neurons from apoptosis. Mice missing the gene encoding neuronal PAS domain protein 3 (NPAS3) are devoid of hippocampal neurogenesis and display malformation and electrophysiological dysfunction of the dentate gyrus. Prolonged administration of P7C3 to npas3/ mice corrected these deficits by normalizing levels of apoptosis of newborn hippocampal neurons. Prolonged administration of P7C3 to aged rats also enhanced neurogenesis in the dentate gyrus, impeded neuron death, and preserved cognitive capacity as a function of terminal aging.
