阿尔茨海默病和非痴呆老年人斑块中β -淀粉样蛋白的分布

Shan-Shan Zhan , Robert Veerhuis , Wouter Kamphorst , Piet Eikelenboom
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引用次数: 82

摘要

最近的研究表明,大脑β淀粉样蛋白(a β)沉积是阿尔茨海默病(AD)病理发展的必要因素,但不是充分因素。在目前的免疫组织化学研究中,我们研究了AD患者中Aβ相关蛋白在大脑新皮层、在Aβ斑块主要为弥漫性的小脑皮层以及在有Aβ斑块的非痴呆患者的大脑新皮层中的分布。结果显示,各组中绝大多数Aβ斑块均出现C1q、C4c、C3d、α1-ACT和载脂蛋白E (ApoE)的免疫标记。ApoJ存在于阿尔茨海默病患者和非痴呆老年人大脑新皮层的β斑块中,但在阿尔茨海默病患者的小脑皮层中几乎不存在。与AD相比,C4Bp和p成分很少出现在非痴呆老年人大脑新皮层的β斑块中。AD小脑弥漫性β斑块中缺乏硫酸肝素蛋白多糖(HSPG)核心蛋白和细胞间粘附分子-1 (ICAM-1)。这些Aβ相关蛋白分布和表达的差异可能由脑区域特定因素(大脑皮层与小脑皮层)和临床状态(痴呆与非痴呆病例)决定。我们认为,除了Aβ肽外,某些Aβ相关蛋白在淀粉样斑块形成和神经原纤维改变的诱导中都是必需的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Distribution of beta amyloid associated proteins in plaques in Alzheimer's disease and in the non-demented elderly

Recent studies have shown that cerebral beta amyloid (Aβ) protein deposition is a necessary, but not sufficient, factor to develop the pathology of Alzheimer's disease (AD). In the present immunohistochemical study, we have investigated in AD the distribution of Aβ associated proteins in the cerebral neocortex, in the cerebellar cortex where Aβ plaques are mainly of the diffuse type, and also in the cerebral neocortex of non-demented patients with Aβ plaques. Results show that immunolabeling for C1q, C4c, C3d, α1-ACT and Apolipoprotein E (ApoE) occurs in the great majority of Aβ plaques in all groups. ApoJ is present in Aβ plaques of the cerebral neocortex in AD and in non-demented elderly, but is almost absent from those of the AD cerebellar cortex. C4Bp and P-component, in contrast to AD, rarely occurs in Aβ plaques of the cerebral neocortex in the non-demented elderly. Heparan sulphate proteoglycan (HSPG) core protein and intercellular adhesion molecule-1 (ICAM-1) are absent in the diffuse Aβ plaques in the AD cerebellum. These differences in distribution and expression of Aβ associated proteins may be determined by brain region specific factors (cerebral cortex versus cerebellar cortex) and clinical state (demented versus non-demented cases). We suggest that, besides Aβ peptide, certain Aβ associated proteins are required for both amyloid plaque formation and for the induction of neurofibrillary changes.

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