Vascular endothelial growth factor in Alzheimer's disease and experimental cerebral ischemia
Vascular endothelial growth factor in Alzheimer's disease and experimental cerebral ischemia
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DOI：
10.1016/s0169-328x(98)00190-9
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发表时间：
1998-11-12
期刊：
影响因子：
--
通讯作者：
Lust, WD
中科院分区：
文献类型：
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作者：
Kalaria, RN;Cohen, DL;Lust, WD
几种生长因子与阿尔茨海默病（AD）的发病机制有关。我们考虑血管内皮生长因子（VEGF）是否参与了与大多数AD病例相关的血管病理。我们观察到增强的VEGF免疫反应性集群的反应性星形胶质细胞在新皮质的受试者与老年对照组相比，AD。在许多大的实质内血管壁和弥漫性血管周围沉积物中也观察到VEGF反应性。此外，我们建立了星形胶质细胞和血管周围的VEGF反应性增强大脑皮质的大鼠进行脑缺血和慢性缺氧，实验条件已知与星形胶质细胞增生和血管生成。我们认为，增加VEGF的反应，也观察到在梗死的人脑组织，涉及代偿机制，以对抗血管不足或减少灌注（少血）明显的AD。(C)1998 Elsevier Science B.V.保留所有权利。
Several growth factors have been implicated in the pathogenesis of Alzheimer's disease (AD). We considered whether the vascular endothelial growth factor (VEGF) is involved in the vascular pathology associated with most cases of AD. We observed enhanced VEGF immunoreactivity in clusters of reactive astrocytes in the neocortex of subjects with AD compared to elderly controls. VEGF reactivity was also noted in walls of many large intraparenchymal vessels and diffuse perivascular deposits. In addition, we established that astrocytic and perivascular VEGF reactivity was enhanced in cerebral cortex of rats subjected to cerebral ischemia and to chronic hypoxia; experimental conditions known to be associated with astrogliosis and angiogenesis. We suggest the increased VEGF reactivity, also observed in infarcted human brain tissue, implicates compensatory mechanisms to counter insufficient vascularity or reduced perfusion (oligemia) apparent in AD. (C) 1998 Elsevier Science B.V. All rights reserved.