神经退行性变
神经毒性
帕金森病
化学
淀粉样蛋白(真菌学)
阳离子聚合
纤维
肽
内生
生物物理学
两亲性
生物化学
疾病
神经科学
细胞生物学
生物
医学
毒性
内科学
无机化学
有机化学
聚合物
共聚物
作者
Jaime Santos,Irantzu Pallarès,Salvador Ventura
标识
DOI:10.1016/j.tibs.2022.02.001
摘要
α-Synuclein (a-syn) oligomers and fibrils are behind neurodegeneration in Parkinson’s disease (PD), but therapeutically targeting them is challenging. Amphipathic and cationic helical peptides inhibit amyloid formation and suppress neurotoxicity by selectively binding the solvent-accessible regions in these toxic species. Can endogenous peptides, like LL-37, constitute a new therapeutic paradigm in PD? α-Synuclein (a-syn) oligomers and fibrils are behind neurodegeneration in Parkinson’s disease (PD), but therapeutically targeting them is challenging. Amphipathic and cationic helical peptides inhibit amyloid formation and suppress neurotoxicity by selectively binding the solvent-accessible regions in these toxic species. Can endogenous peptides, like LL-37, constitute a new therapeutic paradigm in PD?
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