肌萎缩侧索硬化
SOD1
超氧化物歧化酶
氧化应激
化学
活性氧
硫辛酸
蛋白质聚集
胶体金
淀粉样蛋白(真菌学)
突变体
细胞生物学
生物化学
癌症研究
FKBP公司
淀粉样疾病
抗氧化剂
药理学
歧化酶
神经退行性变
药物发现
体外
纳米生物技术
氧化磷酸化
硫辛酸
生物物理学
作者
Pulak Kumar Jana,Sudip Kundu,Rajdip Roy,Dwipanjan Sanyal,Chandan Kumar Ghosh,Snehasis Mishra,Krishnananda Chattopadhyay
标识
DOI:10.1021/acsanm.5c05351
摘要
Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease that affects motor neurons. Mutations in superoxide dismutase 1 (SOD1) cause protein misfolding, amyloid accumulation, and an increase in reactive oxygen species (ROS), which contribute to the disease’s progression. There is currently no cure, and our limited understanding of ALS makes it difficult to develop effective treatments. Gold nanoparticles (GNPs) can cross the blood–brain barrier and are becoming promising tools for drug delivery. Lipoic acid (LA) fights oxidative stress but is poorly absorbed and unstable. In this study, we developed LA-conjugated GNPs (GNPs–LA), which inhibited SOD1 aggregation, reduced ROS production, and minimized cellular damage. The GNPs–LA system showed excellent biocompatibility, offering therapeutic potential for ALS treatment.
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