A central event that underlies the etiology of Alzheimer's disease (AD) is the self-assembly of the amyloid-β (Aβ) peptide into aggregates termed amyloids. Increasing evidence implicates soluble prefibrillar Aβ oligomers in the neurodegeneration and synaptic dysfunction in AD. Recently we introduced a new class of highly promising antagonists of Aβ amyloidogenesis: designed cell-penetrating peptides (CPPs). These CPPs combine the attractive intrinsic properties of peptides (high target specificity and selectivity, biocompatibility, biodegradability, and ease and low cost of production) with potent therapeutic effects (inhibition of Aβ oligomerization, fiber formation, and neurotoxicity) and highly efficient delivery (to target cells and subcellular organelles).

中文翻译：

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用蛋白质对抗蛋白质：淀粉样蛋白β聚集和相关的神经毒性的工程穿透细胞的肽拮抗剂。

阿尔茨海默氏病（AD）的病因基础是一个中心事件，即淀粉样蛋白β（Aβ）肽自组装成称为淀粉样蛋白的聚集体。越来越多的证据表明可溶性原纤维前Aβ寡聚体参与AD的神经变性和突触功能障碍。最近，我们引入了新一类极有希望的Aβ淀粉样蛋白生成拮抗剂：设计的细胞穿透肽（CPPs）。这些CPP结合了肽的诱人内在特性（高靶标特异性和选择性，生物相容性，生物降解性以及生产的简便性和低成本）与强效的治疗作用（抑制Aβ寡聚，纤维形成和神经毒性）和高效的递送（靶细胞和亚细胞器）。