德國亥姆霍茲慕尼黑中心25日發表公報說，德國研究人員在成年鼠腦中發現了能修復受損大腦的神經幹細胞。研究人員稱，如果通過某種方法刺激人腦實現類似的修復過程，將有助於找到醫治老年痴呆症（又稱阿爾茨海默氏症）等腦部疾病的新方法。
公報說，亥姆霍茲慕尼黑中心和慕尼黑大學的研究人員在研究成年鼠前腦的嗅覺信息編碼和處理中心——嗅球時發現，那裡有神經幹細胞，能不斷生成一種被稱為「穀氨酸能中間神經元」的神經細胞。研究人員說，這一發現之所以重要是因為實驗證明，在鼠腦受損傷後，嗅球中的神經幹細胞還能為相鄰的大腦皮層生成新的「穀氨酸能中間神經元」。這些神經細胞能轉移到受損的大腦組織中，並在那裡形成成熟的神經細胞，從而使受損大腦得到修復。
這一發現為探尋老年痴呆症等腦部疾病的醫治方法提供了新思路，目前研究人員正研究鼠腦損傷自我修復過程在人身上是否也能實現。
有關成果已在新一期英國《自然·神經科學》雜誌上發表。（生物谷Bioon.com）
生物谷推薦原始出處：
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.