Kim H S, Lee S H, Kim S S, Kim Y K, Jeong S J, Ma J, Han D H, Cho B K, Suh Y H
Department of Pharmacology, College of Medicine, Seoul National University, Korea.
Neuroreport. 1998 Feb 16;9(3):533-7.
A significant porportion (25%) of patients with Alzheimer's disease (AD) also shows vascular pathology. Recent ultrastructural studies demonstrated characteristic and extensive angio-architectural distortions of cerebral capillaries in AD brains. We examined the expression of APP mRNA isoforms of cerebral cortex after transient ischemia by middle cerebral artery occlusion, using RT-PCR. Neuronal damage and glial fibrillary acidic protein immunohistochemistry were also examined histologically. After transient ischemia, the Kunitz protease inhibitor-bearing isoforms (KPI-APP) were increased whereas APP 695, which lacks KPI domain, was decreased. Neuronal damage and GFAP-immunoreactive astrocytes were also observed. These results show that focal, transient ischemia alters KPI-APP/APP 695 ratio in cerebral cortex and this shift in APP isoforms could be related to neurodegeneration and/or activation of astrocytes during the ischemic process.
很大一部分（25%）阿尔茨海默病（AD）患者也表现出血管病变。最近的超微结构研究表明，AD脑内脑毛细血管存在特征性且广泛的血管结构扭曲。我们通过大脑中动脉闭塞造成短暂性缺血后，使用逆转录聚合酶链反应（RT-PCR）检测大脑皮质中APP mRNA亚型的表达。还通过组织学检查了神经元损伤和胶质纤维酸性蛋白免疫组织化学情况。短暂性缺血后，含库尼茨蛋白酶抑制剂的亚型（KPI-APP）增加，而缺乏KPI结构域的APP 695减少。还观察到了神经元损伤和GFAP免疫反应性星形胶质细胞。这些结果表明，局灶性短暂性缺血会改变大脑皮质中KPI-APP/APP 695的比例，而APP亚型的这种变化可能与缺血过程中的神经退行性变和/或星形胶质细胞激活有关。
