日本一個研究小組以線蟲為對象,，發(fā)現(xiàn)一類名為Wnt的蛋白質(zhì)可以防止腦神經(jīng)細胞之間的正常連接被“誤刪除”。這一成果有望幫助人們理解阿爾茨海默氏癥等腦神經(jīng)變性疾病,。

由東京大學,、九州大學等機構(gòu)科研人員組成的聯(lián)合研究小組在6月28日的網(wǎng)絡(luò)版《自然—神經(jīng)學》雜志上報告說，人腦由超過1000億個神經(jīng)細胞互相連接,，形成復雜的回路,。在人的成長期，腦神經(jīng)細胞延伸出突起,，互相連接,。同時，一些不必要的連接被刪除,，以提高信息傳遞的效率?，F(xiàn)有理論認為，如果這種刪除實施過頭,，傷害到正常的腦神經(jīng)功能,，就會導致腦神經(jīng)變性疾病發(fā)病。

研究人員以只有302個腦神經(jīng)細胞的線蟲為對象,，研究神經(jīng)細胞之間如何互相連接,。研究結(jié)果證實，線蟲也有自動刪除神經(jīng)細胞之間不必要連接的本領(lǐng),。他們發(fā)現(xiàn),，蛋白質(zhì)MBR—1在刪除過程中負責切斷神經(jīng)細胞突起，而蛋白質(zhì)Wnt則在突起被切斷之前附著到神經(jīng)細胞上,，防止必要的神經(jīng)細胞連接被切斷,。研究人員據(jù)此推測，哺乳動物體內(nèi)也有這樣的保護機制,。這一成果將有助于理解阿爾茨海默氏癥,、帕金森氏癥和肌萎縮側(cè)索硬化癥等腦神經(jīng)變性疾病。（生物谷Bioon.com）

生物谷推薦原始出處：

Nature Neuroscience 28 June 2009 | doi:10.1038/nn.2347

A trophic role for Wnt-Ror kinase signaling during developmental pruning in Caenorhabditis elegans

Yu Hayashi1,4, Takaaki Hirotsu2,5, Ryo Iwata3,5, Eriko Kage-Nakadai1,4, Hirofumi Kunitomo3, Takeshi Ishihara2, Yuichi Iino3 & Takeo Kubo1

The molecular mechanism by which neurites are selected for elimination or incorporation into the mature circuit during developmental pruning remains unknown. The trophic theory postulates that local cues provided by target or surrounding cells act to inhibit neurite elimination. However, no widely conserved factor mediating this trophic function has been identified. We found that the developmental survival of specific neurites in Caenorhabditis elegans largely depends on detection of the morphogen Wnt by the Ror kinase CAM-1, which is a transmembrane tyrosine kinase with a Frizzled domain. Mutations in Wnt genes or in cam-1 enhanced neurite elimination, whereas overexpression of cam-1 inhibited neurite elimination in a Wnt-dependent manner. Moreover, mutations in these genes counteracted the effect of a mutation in mbr-1, which encodes a transcription factor that promotes neurite elimination. These results reveal the trophic role of an atypical Wnt pathway and reinforce the classical model of developmental pruning.

1 Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
2 Department of Biology, Graduate School of Science, Kyushu University, Fukuoka, Japan.
3 Deparment of Biophysics and Biochemistry, Graduate School of Science, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
4 Present address: Laboratory for Behavioral Genetics, RIKEN Brain Science Institute, Saitama, Japan (Y.H.), and Department of Physiology, Tokyo Women's 5 Medical University School of Medicine, Shinjuku-ku, Tokyo, Japan (E.K.-N.).
6 These authors contributed equally to this work.