Kalaria R N, Bhatti S U, Palatinsky E A, Pennington D H, Shelton E R, Chan H W, Perry G, Lust W D
Department of Neurology, Case Western Reserve University, Cleveland, OH 44106.
Neuroreport. 1993 Feb;4(2):211-4. doi: 10.1097/00001756-199302000-00025.
We used various antibodies to the beta amyloid precursor protein (APP) of Alzheimer's disease to study changes in the cellular distribution of APP in experimental ischemic brain injury. In contrast to sham operated controls, rats with repeated reversible occlusions of one middle cerebral artery showed striking APP reactivity in astrocytic processes in perifocal regions and white matter tracts. Dystrophic axons and neurons with accumulated APP were also evident in the ipsilateral neocortex and hippocampus. Such changes were also apparent in rats subjected to partial forebrain ischemia by bilateral occlusion of the carotid arteries. Our studies suggest that focal ischemic insults or chronic hypoperfusion leads to increased accumulation of APP in surviving brain cells that may pertain to enhanced beta amyloid deposition in Alzheimer's disease.
我们使用了多种针对阿尔茨海默病β淀粉样前体蛋白（APP）的抗体，来研究实验性缺血性脑损伤中APP细胞分布的变化。与假手术对照组相比，反复可逆性闭塞一侧大脑中动脉的大鼠在病灶周围区域和白质束的星形胶质细胞突起中显示出显著的APP反应性。同侧新皮层和海马体中，具有累积APP的营养不良轴突和神经元也很明显。在通过双侧颈总动脉闭塞进行部分前脑缺血的大鼠中，这种变化也很明显。我们的研究表明，局灶性缺血性损伤或慢性灌注不足会导致存活脑细胞中APP的积累增加，这可能与阿尔茨海默病中β淀粉样蛋白沉积增加有关。
