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淀粉样蛋白、痴呆与阿尔茨海默病。

Amyloid, dementia and Alzheimer's disease.

作者信息

Hyman B T, Tanzi R E

机构信息

Department of Neurology, Massachusetts General Hospital, Boston.

出版信息

Curr Opin Neurol Neurosurg. 1992 Feb;5(1):88-93.

PMID:1623244
Abstract

Senile plaques (SP) and neurofibrillary tangles (NFT) are the major histopathological changes that occur in Alzheimer's disease (AD). How these two different types of lesions are related to each other and to the dementia of AD is unknown. Recent studies lead to paradoxical conclusions: NFT and neuronal alterations such as synapse loss are much more closely related to the symptoms of dementia than are SP. However, mutations in the beta-amyloid protein of SP have been found in some patients with familial AD, suggesting that an abnormality in amyloid causes the development of SP, NFT and AD dementia. Examination of transgenic animals that produce amyloid precursor protein (APP), or altered forms of APP, may lead to the development of an animal model of AD, and ultimately to answers that link amyloid production to neuronal alterations, and cognitive impairments.

摘要

老年斑(SP)和神经原纤维缠结(NFT)是阿尔茨海默病(AD)中出现的主要组织病理学变化。这两种不同类型的病变如何相互关联以及与AD痴呆症的关系尚不清楚。最近的研究得出了相互矛盾的结论:与老年斑相比,神经原纤维缠结和神经元改变(如突触丧失)与痴呆症状的关系更为密切。然而,在一些家族性AD患者中发现了老年斑β-淀粉样蛋白的突变,这表明淀粉样蛋白异常会导致老年斑、神经原纤维缠结和AD痴呆症的发展。对产生淀粉样前体蛋白(APP)或APP变体形式的转基因动物进行研究,可能会导致AD动物模型的建立,并最终找到将淀粉样蛋白产生与神经元改变及认知障碍联系起来的答案。

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