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[阿尔茨海默病中的细胞病变:结构与分子分析]

[Cellular lesions in Alzheimer's disease: structural and molecular analysis].

作者信息

Brion J P

出版信息

Bull Mem Acad R Med Belg. 1992;147(11-12):481-9; discussion 490-1.

PMID:1341572
Abstract

Neurofibrillary tangles and senile plaques are the characteristic neuropathological lesions of Alzheimer's disease. Neurofibrillary tangles are composed of a microtubule-associated protein, the tau protein. This protein plays a role in the development of neuronal polarity and the stabilisation of microtubules. In Alzheimer's disease, tau proteins are abnormally phosphorylated on several sites. This abnormal phosphorylation might induce the modifications of the microtubule network observed in affected neurones. The main component of the senile plaque is an amyloid deposit made of a polypeptide (beta/A4 amyloid) which derives from a larger precursor. The overexpression of this precursor in experimental models or mutations of its gene leads to the development of neuropathological lesions. The relationships between cytoskeletal abnormalities and beta/A4 amyloid are further discussed.

摘要

神经原纤维缠结和老年斑是阿尔茨海默病典型的神经病理学病变。神经原纤维缠结由一种微管相关蛋白——tau蛋白组成。这种蛋白在神经元极性的发展和微管的稳定中发挥作用。在阿尔茨海默病中,tau蛋白在多个位点发生异常磷酸化。这种异常磷酸化可能会导致在受影响神经元中观察到的微管网络的改变。老年斑的主要成分是一种由较大前体衍生而来的多肽(β/A4淀粉样蛋白)形成的淀粉样沉积物。该前体在实验模型中的过度表达或其基因突变会导致神经病理学病变的发展。文中进一步讨论了细胞骨架异常与β/A4淀粉样蛋白之间的关系。

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