Plaque-associated α-synuclein (NACP) pathology in aged transgenic mice expressing amyloid precursor protein

被引：54

作者：

Yang, FS

Uéda, K

Chen, PP

Ashe, KH

Cole, GM

机构：

[1] VAMC, Ctr Geriatr Res Educ & Clin 11E, Sepulveda, CA 91343 USA

[2] Univ Calif Los Angeles, Dept Med, Sepulveda, CA 91343 USA

[3] Univ Calif Los Angeles, Dept Neurol, Sepulveda, CA 91343 USA

[4] Univ Minnesota, Ctr Clin & Mol Neurobiol, Dept Neurol, Minneapolis, MN 55455 USA

[5] Univ Minnesota, Ctr Clin & Mol Neurobiol, Dept Neurosci, Minneapolis, MN 55455 USA

[6] Tokyo Inst Psychiat, Dept Neurochem, Setagaya Ku, Tokyo 1568585, Japan

来源：

BRAIN RESEARCH | 2000年 / 853卷 / 02期

关键词：

alpha-synuclein; amyloid precursor; transgenic; Alzheimer's; Parkinson's; Lewy;

D O I：

10.1016/S0006-8993(99)02207-6

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Patients with the Lewy body variant (LBV) of Alzheimer's disease (AD) have ubiquitinated intraneuronal and neuritic accumulations of alpha-synuclein and show less neuron loss and tau pathology than other AD patients. Aged Tg2576 transgenic mice overexpressing human beta APP695, KM670/671NL have limited neuron loss and tau pathology, but frequent ubiquitin- and alpha-synuclein-positive, tau-negative neurites resembling those seen in the LBV of AD. (C) 2000 Elsevier Science B.V. All rights reserved.

引用

收藏

页码：381 / 383

页数：3

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