Serbinek Daniela, Ullrich Celine, Pirchl Michael, Hochstrasser Tanja, Schmidt-Kastner Rainald, Humpel Christian
Laboratory of Psychiatry and Exp. Alzheimer's Research, Department of Psychiatry and Psychotherapy, Innsbruck Medical University, Anichstra beta e 35, 6020 Innsbruck, Austria.
Cardiovasc Psychiatry Neurol. 2010;2010:106123. doi: 10.1155/2010/106123. Epub 2010 May 24.
Alzheimer's disease is a severe chronic neurodegenerative disorder characterized by beta-amyloid plaques, tau pathology, cerebrovascular damage, inflammation, reactive gliosis, and cell death of cholinergic neurons. The aim of the present study is to test whether the glia-derived molecule S100b can counteract neurodegeneration of cholinergic neurons after oxygen-glucose deprivation (OGD) in organotypic brain slices of basal nucleus of Meynert. Our data showed that 3 days of OGD induced a marked decrease of cholinergic neurons (60% of control), which could be counteracted by 50 mug/mL recombinant S100b. The effect was dose and time dependent. Application of nerve growth factor or fibroblast growth factor-2 was less protective. C-fos-like immunoreactivity was enhanced 3 hours after OGD indicating metabolic stress. We conclude that S100b is a potent neuroprotective factor for cholinergic neurons during ischemic events.
阿尔茨海默病是一种严重的慢性神经退行性疾病，其特征为β-淀粉样斑块、tau病理改变、脑血管损伤、炎症、反应性胶质增生以及胆碱能神经元死亡。本研究的目的是检测神经胶质衍生分子S100b是否能够对抗梅纳特基底核器官型脑片中氧-葡萄糖剥夺（OGD）后胆碱能神经元的神经退行性变。我们的数据显示，3天的OGD诱导胆碱能神经元显著减少（为对照的60%），而50μg/mL重组S100b可对抗这一现象。该效应具有剂量和时间依赖性。应用神经生长因子或成纤维细胞生长因子-2的保护作用较弱。OGD后3小时，C-fos样免疫反应性增强，表明存在代谢应激。我们得出结论，S100b是缺血事件期间胆碱能神经元的一种有效的神经保护因子。
