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β-折叠破坏肽在淀粉样变性大鼠脑模型中抑制纤维形成:对阿尔茨海默病治疗的意义。

Beta-sheet breaker peptides inhibit fibrillogenesis in a rat brain model of amyloidosis: implications for Alzheimer's therapy.

作者信息

Soto C, Sigurdsson E M, Morelli L, Kumar R A, Castaño E M, Frangione B

机构信息

Department of Pathology, New York University Medical Center, New York 10016, USA.

出版信息

Nat Med. 1998 Jul;4(7):822-6. doi: 10.1038/nm0798-822.

Abstract

Inhibition of cerebral amyloid beta-protein deposition seems to be an important target for Alzheimer's disease therapy. Amyloidogenesis could be inhibited by short synthetic peptides designed as beta-sheet breakers. Here we demonstrate a 5-residue peptide that inhibits amyloid beta-protein fibrillogenesis, disassembles preformed fibrils in vitro and prevents neuronal death induced by fibrils in cell culture. In addition, the beta-sheet breaker peptide significantly reduces amyloid beta-protein deposition in vivo and completely blocks the formation of amyloid fibrils in a rat brain model of amyloidosis. These findings may provide the basis for a new therapeutic approach to prevent amyloidosis in Alzheimer's disease.

摘要

抑制大脑β-淀粉样蛋白沉积似乎是阿尔茨海默病治疗的一个重要靶点。淀粉样蛋白生成可被设计为β-折叠破坏剂的短合成肽所抑制。在此,我们展示了一种五肽,它能抑制β-淀粉样蛋白的纤维形成,在体外拆解预先形成的纤维,并在细胞培养中防止由纤维诱导的神经元死亡。此外,β-折叠破坏剂肽在体内显著减少β-淀粉样蛋白沉积,并在淀粉样变性大鼠脑模型中完全阻断淀粉样纤维的形成。这些发现可能为预防阿尔茨海默病淀粉样变性的新治疗方法提供依据。

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