日本一个研究小组以线虫为对象，发现一类名为Wnt的蛋白质可以防止脑神经细胞之间的正常连接被“误删除”。这一成果有望帮助人们理解阿尔茨海默氏症等脑神经变性疾病。
由东京大学、九州大学等机构科研人员组成的联合研究小组在6月28日的网络版《自然—神经学》杂志上报告说，人脑由超过1000亿个神经细胞互相连接，形成复杂的回路。在人的成长期，脑神经细胞延伸出突起，互相连接。同时，一些不必要的连接被删除，以提高信息传递的效率。现有理论认为，如果这种删除实施过头，伤害到正常的脑神经功能，就会导致脑神经变性疾病发病。
研究人员以只有302个脑神经细胞的线虫为对象，研究神经细胞之间如何互相连接。研究结果证实，线虫也有自动删除神经细胞之间不必要连接的本领。他们发现，蛋白质MBR—1在删除过程中负责切断神经细胞突起，而蛋白质Wnt则在突起被切断之前附着到神经细胞上，防止必要的神经细胞连接被切断。研究人员据此推测，哺乳动物体内也有这样的保护机制。这一成果将有助于理解阿尔茨海默氏症、帕金森氏症和肌萎缩侧索硬化症等脑神经变性疾病。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
