Miyakawa T, Uehara Y, Desaki J, Kimura T, Kuramoto R
Department of Neuropsychiatry, Kumamoto University Medical School, Japan.
Jpn J Psychiatry Neurol. 1988 Dec;42(4):819-24. doi: 10.1111/j.1440-1819.1988.tb01171.x.
The pathological changes of microvessels in the cerebral cortex in Alzheimer's disease were examined at the ultrastructural level. With transmission electron microscopy (TEM), the endothelial cells of many capillaries and their pericytes exhibited atrophy and swelling with a narrowed lumen. The capillary basal laminas were thickened and tortuous. After isolation of the microvessels by ultrasonic treatment and collagenase digestion, the vascular wall structure was viewed by scanning electron microscopy (SEM). Most of the terminal arterioles had smooth muscle cells with an irregular shape and arrangement and often showed a series of focal constrictions. In some areas, the capillaries were arrayed in a bundle and terminated with tapered ends. Associated with the microvessels were fine filaments which may represent amyloid fibrils. The findings indicate that diffuse atrophy and the deletion of nerve cells in the cerebral cortex might be caused, at least partly, by a circulatory disturbance through the pathomorphologically changed microvessels.
在超微结构水平上检查了阿尔茨海默病大脑皮质微血管的病理变化。通过透射电子显微镜（TEM）观察到，许多毛细血管的内皮细胞及其周细胞出现萎缩和肿胀，管腔变窄。毛细血管基膜增厚且迂曲。通过超声处理和胶原酶消化分离微血管后，用扫描电子显微镜（SEM）观察血管壁结构。大多数终末小动脉的平滑肌细胞形状和排列不规则，常出现一系列局灶性狭窄。在一些区域，毛细血管成束排列，末端呈锥形。与微血管相关的是细丝，可能代表淀粉样纤维。这些发现表明，大脑皮质中神经细胞的弥漫性萎缩和缺失可能至少部分是由形态学改变的微血管引起的循环障碍所致。
