Couratier P, Lesort M, Condamines O, Mourton-Gilles C, Delacourte A, Hugon J
Unite de Neurobiologie et Pathologie Cellulaire, Laboratoire d'Histologie, Faculte de Medecine, Limoges Cedex, France.
Neurosci Lett. 1996 Jan 26;203(3):155-8. doi: 10.1016/0304-3940(96)12302-8.
One of the hallmarks of Alzheimer's disease (AD) is neurofibrillary degeneration which results from the aggregation of phosphorylated tau proteins into paired helical filament (PHF) structures. AD2 is a new monoclonal antibody raised against PHF tau which detects neurofibrillary tangles in AD brain. In primary neuronal cultures, phorbol ester treatment induced a time- and dose-dependent increase in AD2 immunoreactivity quantified by laser confocal microscopy and immunoblottings. Alkaline phosphatase treatment reversed these immunocytochemical changes. These results suggest that the modifications of neuronal metabolism induced by phorbol ester including protein kinase C activation produce an increase in phosphorylated tau immunoreactivity.
阿尔茨海默病（AD）的标志之一是神经原纤维变性，它是由磷酸化tau蛋白聚集成双螺旋丝（PHF）结构所致。AD2是一种针对PHF tau产生的新型单克隆抗体，可检测AD大脑中的神经原纤维缠结。在原代神经元培养中，佛波酯处理通过激光共聚焦显微镜和免疫印迹法检测，可使AD2免疫反应性呈时间和剂量依赖性增加。碱性磷酸酶处理可逆转这些免疫细胞化学变化。这些结果表明，佛波酯诱导的神经元代谢改变，包括蛋白激酶C激活，会使磷酸化tau免疫反应性增加。
