德国亥姆霍兹慕尼黑中心25日发表公报说，德国研究人员在成年鼠脑中发现了能修复受损大脑的神经干细胞。研究人员称，如果通过某种方法刺激人脑实现类似的修复过程，将有助于找到医治老年痴呆症（又称阿尔茨海默氏症）等脑部疾病的新方法。
公报说，亥姆霍兹慕尼黑中心和慕尼黑大学的研究人员在研究成年鼠前脑的嗅觉信息编码和处理中心——嗅球时发现，那里有神经干细胞，能不断生成一种被称为“谷氨酸能中间神经元”的神经细胞。研究人员说，这一发现之所以重要是因为实验证明，在鼠脑受损伤后，嗅球中的神经干细胞还能为相邻的大脑皮层生成新的“谷氨酸能中间神经元”。这些神经细胞能转移到受损的大脑组织中，并在那里形成成熟的神经细胞，从而使受损大脑得到修复。
这一发现为探寻老年痴呆症等脑部疾病的医治方法提供了新思路，目前研究人员正研究鼠脑损伤自我修复过程在人身上是否也能实现。
有关成果已在新一期英国《自然·神经科学》杂志上发表。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature Neuroscience 12, 1524 - 1533 (2009) 1 November 2009 | doi:10.1038/nn.2416
Adult generation of glutamatergic olfactory bulb interneurons
Monika S Brill1,2,3,10, Jovica Ninkovic2,3,10, Eleanor Winpenny4,10, Rebecca D Hodge5,10, Ilknur Ozen4, Roderick Yang5, Alexandra Lepier1, Sergio Gascón1,2, Ferenc Erdelyi6, Gabor Szabo6, Carlos Parras7,9, Francois Guillemot7, Michael Frotscher8, Benedikt Berninger1,2, Robert F Hevner5, Olivier Raineteau4,9 & Magdalena G?tz1,3
The adult mouse subependymal zone (SEZ) harbors neural stem cells that are thought to exclusively generate GABAergic interneurons of the olfactory bulb. We examined the adult generation of glutamatergic juxtaglomerular neurons, which had dendritic arborizations that projected into adjacent glomeruli, identifying them as short-axon cells. Fate mapping revealed that these originate from Neurog2- and Tbr2-expressing progenitors located in the dorsal region of the SEZ. Examination of the progenitors of these glutamatergic interneurons allowed us to determine the sequential expression of transcription factors in these cells that are thought to be hallmarks of glutamatergic neurogenesis in the developing cerebral cortex and adult hippocampus. Indeed, the molecular specification of these SEZ progenitors allowed for their recruitment into the cerebral cortex after a lesion was induced. Taken together, our data indicate that SEZ progenitors not only produce a population of adult-born glutamatergic juxtaglomerular neurons, but may also provide a previously unknown source of progenitors for endogenous repair.
1 Department of Physiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, Munich, Germany.
2 Institute for Stem Cell Research, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany.
3 Munich Center for Integrated Protein Science CiPSM, Munich, Germany.
4 Cambridge Centre for Brain Repair, Robinson Way, Cambridge, UK.
5 Departments of Neurological Surgery and Pathology, University of Washington, Seattle Children's Hospital Research Institute, Seattle, Washington, USA.
6 Laboratory of Molecular Biology and Genetics, Institute of Experimental Medicine, Budapest, Hungary.
7 Division of Molecular Neurobiology, Medical Research Council—National Institute for Medical Research, London, UK.
8 Insitute of Anatomy and Cell Biology, University of Freiburg, Freiburg, Germany.
9 Present address: Brain Research Institute, University of Zürich/ETH, Zürich, Switzerland (O.R.), INSERM U711, Biologie des Interactions Neurones/Glie, H?pital de la Pitié-Salpêtrière, Batiment de la Pharmacie, Paris, France (C.P.).
These authors contributed equally to this work.
