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1. 发明授权

US07276643B2 Transgenic animals, cell lines derived therefrom, and methods for screening for anti-amyloidogenic agents 有权
标题翻译：转基因动物，由其衍生的细胞系，以及筛选抗淀粉样变性剂的方法
公开(公告)号：US07276643B2
公开(公告)日：2007-10-02
申请号：US10204337
申请日：2001-02-20
申请人： Eliezer Masliah , Edward Rockenstein , Hersey Mallory, legal representative
发明人： Margaret Mallory, deceased
IPC分类号： A01K67/027 , G01N33/00 , C12N5/02
CPC分类号： C12N15/8509 , A01K67/0275 , A01K67/0276 , A01K67/0278 , A01K2207/15 , A01K2217/00 , A01K2217/05 , A01K2217/075 , A01K2227/105 , A01K2267/0312 , A01K2267/0318 , A61K38/00 , A61K48/00 , C07K14/47 , C07K14/4711 , C12N2830/008
摘要： The methodologies of the present invention demonstrate that a critical balance between pro- and anti-amyloidogenic molecules exists that regulates amyloid formation and cell death in Alzheimer's disease and Parkinson's disease. β-Synuclein, the non-amyloidogenic homologue of α-synuclein, is a negative modulator of α-synuclein and Aβ aggregation, having neuroprotective properties against α-synuclein and Aβ neurotoxicity and that β-synuclein and therapeutic agents derived therefrom block amyloidogenesis and neurodegeneration in vivo. The method of the present invention establishes that β-synuclein blocks Aβ aggregation either by direct inhibition of Aβ amyloidogenesis or indirectly via either α-synuclein or its 35 a.a. NAC region, inferring neuroprotective characteristics within the effected cells. The generation of a transgenic mouse line and a cell system overexpressing α-synuclein characterizes the mechanisms by which β-synuclein blocks α-synuclein and Aβ aggregation and that this mechanism offers protection to the cell against amyloid formation as seen in the pathologies of Alzheimer's disease and Parkinson's disease.
摘要翻译：本发明的方法证明，存在调节淀粉样蛋白形成和阿尔茨海默病和帕金森病中的细胞死亡的促淀粉样变性分子和抗淀粉样蛋白形成分子之间的关键平衡。 β-共核蛋白是α-突触核蛋白的非淀粉样变性同源物，是α-突触核蛋白和Abeta聚集的负调节剂，具有针对α-突触核蛋白和Abeta神经毒性的神经保护性质，并且β-突触核蛋白和衍生自其的治疗剂阻断淀粉样变性和神经变性体内。本发明的方法确定了β-突触核蛋白通过直接抑制Aβ淀粉样变性或间接通过α-突触核蛋白或其αααα阻断Aβ聚集。 NAC区域，推断受影响细胞内的神经保护特征。转基因小鼠系和过表达α-突触核蛋白的细胞系统的产生表征β-突触核蛋白阻断α-突触核蛋白和Abeta聚集的机制，并且该机制为细胞抵抗淀粉样蛋白形成提供了保护，如阿尔茨海默病病理学和帕金森病。

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