Töpper R, Gehrmann J, Banati R, Schwarz M, Block F, Noth J, Kreutzberg G W
Max-Planck-Institute of Psychiatry, Department of Neuromorphology, Martinsried, Germany.
Acta Neuropathol. 1995;89(1):23-8. doi: 10.1007/BF00294255.
Clinical and experimental data have indicated an up-regulation of amyloid precursor protein (APP) after various types of CNS injury. In the present study the cellular source of lesion-induced APP has been investigated in a neurotoxic CNS model. Quinolinic acid injection into the striatum results in neuronal degeneration, while glial cells survive. APP immunoreactivity was detected in glial cells starting at postoperative day 3 and persisted until day 21, the last time point studied. Double immunocytochemistry identified the majority of APP-immunoreactive cells as glial fibrillary acidic protein-immunoreactive astrocytes. There was no evidence of amyloid fibril deposition during this time. It is concluded that following excitotoxic neuronal degneration APP is mainly produced by reactive astrocytes in the lesioned area.
临床和实验数据表明，在各种类型的中枢神经系统损伤后，淀粉样前体蛋白（APP）会出现上调。在本研究中，已在神经毒性中枢神经系统模型中研究了损伤诱导的APP的细胞来源。向纹状体注射喹啉酸会导致神经元变性，而胶质细胞存活。术后第3天开始在胶质细胞中检测到APP免疫反应性，并持续到第21天，即研究的最后一个时间点。双重免疫细胞化学鉴定出大多数APP免疫反应性细胞为胶质纤维酸性蛋白免疫反应性星形胶质细胞。在此期间没有淀粉样纤维沉积的证据。结论是，在兴奋性毒性神经元变性后，APP主要由损伤区域的反应性星形胶质细胞产生。
