Vascular basement membrane components and the lesions of Alzheimer's disease: light and electron microscopic analyses.
Vascular basement membrane components and the lesions of Alzheimer's disease: light and electron microscopic analyses.
复制标题
血管基底膜成分和阿尔茨海默病的病变：光和电子显微镜分析。
DOI：
10.1002/jemt.1070280305
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发表时间：
1994
影响因子：
2.5
通讯作者：
Barron,E
中科院分区：
文献类型：
--
作者：
Perlmutter,LS;Myers,MA;Barron,E
阿尔茨海默病 (AD) 是几种全身性和脑部疾病之一，涉及称为淀粉样蛋白的纤维状蛋白的异常沉积。所有淀粉样蛋白都具有相同的构象和染色特征，以及与常驻组织巨噬细胞和两种细胞外基质成分[硫酸乙酰肝素蛋白聚糖 (HSPG) 和淀粉样蛋白 P 成分] 的关联。血管、肾小球和雪旺细胞基底膜病变已在多种形式的淀粉样变性中被记录，并且在这些疾病中淀粉样原纤维常常融合到基底膜并从基底膜突出。本报告展示了 AD 尸检样本中血管基底膜 (VBM) 的变化，并详细介绍了所用的方法。电子显微镜揭示了淀粉样蛋白原纤维与 VBM 的融合，以及在没有淀粉样蛋白积累的情况下 VBM 的变化。双标记和预嵌入免疫电镜技术证明了淀粉样蛋白 P 成分和 VBM 成分与淀粉样蛋白的共定位，并且还揭示了淀粉样蛋白 P 成分并不定位于大脑 VBM。最后，一种新型相关光学/电子显微镜技术证明了淀粉样蛋白 P 成分与大脑驻留组织巨噬细胞（小胶质细胞）之间的关联。总而言之，这些数据表明淀粉样蛋白形成的物理化学过程，而不是淀粉样蛋白沉积，可能是 VBM 病理学的原因。 © 1994 Wiley-Liss, Inc.
Alzheimer's disease (AD) is one of several systemic and cerebral diseases that involve the abnormal deposition of fibrillar proteins called amyloids. All amyloids share conformational and staining characteristics, as well as an association with resident tissue macrophages and two extracellular matrix components [heparan sulfate proteoglycan (HSPG) and amyloid P component]. Vascular, glomerular, and Schwann cell basement membrane pathologies have been documented in many forms of amyloidosis, and often amyloid fibrils fuse to and project from the basement membrane in these diseases. The present report demonstrates the vascular basement membrane (VBM) alterations in AD autopsy samples, and details the methodologies used.Electron microscopy reveals the fusion of amyloid fibrils with the VBM and the alteration of the VBM in the absence of amyloid accumulation. Double‐labelling and pre‐embed immuno‐electron microscopy techniques demonstrate the colocalization of amyloid P component and VBM components with amyloid, and also reveal that amyloid P component is not localized to the cerebral VBM. Finally, a novel correlative light/electron microscopy technique demonstrates the association between amyloid P component and cerebral resident tissue macrophages, the microglia. Taken together, these data suggest that the physicochemical processes of amyloid formation, rather than amyloid deposition, may be responsible for VBM pathology. © 1994 Wiley‐Liss, Inc.