Scheibel A B, Duong T H, Tomiyasu U
Department of Anatomy, UCLA Medical Center 90024.
Alzheimer Dis Assoc Disord. 1987;1(1):19-37. doi: 10.1097/00002093-198701000-00004.
Structural analysis of the capillary plexus in the brains of 5 patients with clinical and neuropathological diagnosis of Senile Dementia, Alzheimer Type, revealed a group of striking physical alterations compared with tissue specimens from 5 age-matched controls. Capillary walls were thickened with irregular lumpy, nodulated contours which appeared due, in part, to infiltration of the vascular wall with rounded cell-like bodies. In some cases, these resembled the perikarya of pericytes or monocytes, or their protoplasmic extensions, which were often filled with lipids. In each case, there was no trace of the perivascular neural plexus which regularly invests the microvasculature of the brain parenchyma. The loss of this neural plexus, believed to originate largely from locus ceruleus and the basal forebrain, may be related to the changes in capillary wall structure, and these, in turn, may lead to profound alterations in blood-brain barrier function. We suggest that this subcortically induced denervation microangiopathy may serve as a pathogenic factor in the development of SDAT.
对5例临床和神经病理学诊断为阿尔茨海默型老年痴呆症患者大脑中的毛细血管丛进行结构分析，结果显示，与5例年龄匹配的对照组织标本相比，出现了一组显著的物理改变。毛细血管壁增厚，轮廓不规则呈块状、结节状，部分原因是血管壁被圆形细胞样物体浸润。在某些情况下，这些物体类似于周细胞或单核细胞的胞体，或它们的原生质延伸物，这些延伸物通常充满脂质。在每种情况下，均未发现正常情况下包绕脑实质微血管的血管周围神经丛的踪迹。据信，这种神经丛主要起源于蓝斑和基底前脑，其缺失可能与毛细血管壁结构的变化有关，而这些变化反过来可能导致血脑屏障功能的深刻改变。我们认为，这种皮质下诱导的去神经支配微血管病可能是SDAT发病的一个致病因素。
