Suppr超能文献

在阿尔茨海默病中,营养不良性神经突浸润细胞外神经原纤维缠结。

Dystrophic neurites infiltrate extracellular neurofibrillary tangles in Alzheimer disease.

作者信息

Vande Weghe J, Cras P, Kawai M, Siedlak S L, Tabaton M, Greenberg B, Perry G

机构信息

Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106.

出版信息

Brain Res. 1991 Sep 27;560(1-2):303-5. doi: 10.1016/0006-8993(91)91247-x.

Abstract

The neurotrophic activity of beta-amyloid protein (beta-AP) has been suggested to be responsible for the dystrophic neurites that surround beta-AP deposits in senile plaques of Alzheimer disease. The recent finding that neurofibrillary tangles (NFT) that remain as remnants in the extracellular space (E-NFT) after the death of the neuron contain beta-AP, suggested that dystrophic neurites might also be associated with E-NFT. In this study, we use a probe for E-NFT, basic fibroblast growth factor (bFGF)-binding to show that E-NFT do contain dystrophic neurites. Since these neurites contain the amyloid precursor protein whose cleavage can lead to beta-AP, they may also play a role in further beta-AP deposition in the E-NFT.

摘要

β-淀粉样蛋白(β-AP)的神经营养活性被认为与阿尔茨海默病老年斑中围绕β-AP沉积物的营养不良性神经突有关。最近的研究发现,神经元死亡后留在细胞外空间的神经原纤维缠结(NFT)(E-NFT)含有β-AP,这表明营养不良性神经突也可能与E-NFT有关。在本研究中,我们使用一种针对E-NFT的探针,即碱性成纤维细胞生长因子(bFGF)结合来表明E-NFT确实含有营养不良性神经突。由于这些神经突含有淀粉样前体蛋白,其裂解可导致β-AP,它们可能也在E-NFT中进一步的β-AP沉积中发挥作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验