Novel compound VB-037 inhibits Aβ aggregation and promotes neurite outgrowth through enhancement of HSP27 and reduction of P38 and JNK-mediated inflammation in cell models for Alzheimer's disease

The pathogenesis of Alzheimer's disease (AD) is involved in the aggregation of misfolded amyloid β (Aβ), which upregulates the activity of acetylcholinesterase (AChE), increases the production of reactive oxygen species (ROS), enhances neuroinflammation, and eventually leads to neuronal death....

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Veröffentlicht in:	Neurochemistry international 2019-05, Vol.125, p.175-186
Hauptverfasser:	Chiu, Ya-Jen, Hsieh, Yu-Hsuan, Lin, Te-Hsien, Lee, Guan-Chiun, Hsieh-Li, Hsiu Mei, Sun, Ying-Chieh, Chen, Chiung-Mei, Chang, Kuo-Hsuan, Lee-Chen, Guey-Jen
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer's disease Amyloid beta-Peptides - antagonists & inhibitors Amyloid beta-Peptides - metabolism Animals Aβ aggregation Cell Line Curcumin - pharmacology HSP27 Heat-Shock Proteins - metabolism Humans Inflammation Mediators - antagonists & inhibitors Inflammation Mediators - metabolism MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - physiology Mice Neuronal Outgrowth - drug effects Neuronal Outgrowth - physiology p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - metabolism P38/JNK signaling pathways Protein Aggregates - drug effects Protein Aggregates - physiology Quinolines - chemistry Quinolines - pharmacology Quinolines - therapeutic use Synthetic quinoline derivatives Therapeutics
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