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在阿尔茨海默病大脑中,P3β-淀粉样肽具有独特且可能致病的免疫组化特征。

P3 beta-amyloid peptide has a unique and potentially pathogenic immunohistochemical profile in Alzheimer's disease brain.

作者信息

Higgins L S, Murphy G M, Forno L S, Catalano R, Cordell B

机构信息

Scios Nova Inc., Mountain View, California 94043, USA.

出版信息

Am J Pathol. 1996 Aug;149(2):585-96.

Abstract

The presence of beta-amyloid in brain tissue is characteristic of Alzheimer's disease (AD). A naturally occurring derivative of the beta-amyloid peptide, p3, possesses all of the structural determinants required for fibril assembly and neurotoxicity. p3-specific antibodies were used to examine the distribution of this peptide in brain. p3 reactivity was absent or sparse in aged non-AD brains but was prevalent in selected areas of AD brain in diffuse deposits and in a subset of dystrophic neurites. p3-reactive dystrophic neurites were found both independent in the neuropil and associated with plaques. Little or no reactivity was observed to amyloid cores in classical plaques or to amyloid in the cerebral vasculature. The exclusive appearance of p3 reactivity in AD brain plus the selective localization of p3 reactivity to abnormal structures in the temporal lobe limbic system suggests that p3 may be a contributing factor to AD pathology.

摘要

脑组织中β-淀粉样蛋白的存在是阿尔茨海默病(AD)的特征。β-淀粉样肽的一种天然衍生物p3,具备原纤维组装和神经毒性所需的所有结构决定因素。使用p3特异性抗体来检测该肽在脑中的分布。在老年非AD脑内,p3反应性缺失或稀少,但在AD脑的特定区域,在弥漫性沉积物以及营养不良性神经突的一个亚群中普遍存在。p3反应性营养不良性神经突既独立存在于神经毡中,也与斑块相关。在经典斑块的淀粉样核心或脑脉管系统的淀粉样蛋白中,未观察到或仅观察到极少的反应性。p3反应性在AD脑中的独特出现,加上p3反应性在颞叶边缘系统异常结构中的选择性定位,表明p3可能是AD病理学的一个促成因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f10/1865300/35404cc08e3c/amjpathol00032-0238-a.jpg

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