Recent advances of small molecule JNK3 inhibitors for Alzheimer?s disease

被引：14

作者：

Qin, Pengxia ^{[1
]}

Ran, Yingying ^{[1
]}

Liu, Yujing ^{[1
]}

Wei, Chao ^{[1
]}

Luan, Xiaoyi ^{[1
]}

Niu, Haoqian ^{[1
]}

Peng, Jie ^{[1
]}

Sun, Jie ^{[1
]}

Wu, Jingde ^{[1
]}

机构：

[1] Shandong Univ, Cheeloo Coll Med, Sch Pharmaceut Sci, Dept Med Chem,Key Lab Chem Biol,Minist Educ, Jinan 250012, Peoples R China

来源：

BIOORGANIC CHEMISTRY | 2022年 / 128卷

关键词：

JNK3; inhibitors; Alzheimer?s disease; A; Tau; Inflammation; Structure -activity relationship; N-TERMINAL KINASE; ACTIVATED PROTEIN-KINASE; AMYLOID BETA-PEPTIDE; C-JUN; NEUROPROTECTIVE ACTION; BIOLOGICAL EVALUATION; SYNAPTIC PLASTICITY; MAPK SCAFFOLD; TAU; POTENT;

D O I：

10.1016/j.bioorg.2022.106090

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

C-Jun N-terminal kinase (JNK) is a member of mitogen-activated protein kinases (MAPKs) family, with three isoforms, JNK1, JNK2 and JNK3. Alzheimer's disease (AD) is a neurological disorder and the most common type of dementia. Two well-established AD pathologies are the deposition of A beta amyloid plaques and neurofibrillary tangles caused by Tau hyperphosphorylation. JNK3 is involved in forming amyloid A beta and neurofibrillary tangles, suggesting that JNK3 may represent a target to develop treatments for AD. Therefore, this review will discuss the roles of JNK3 in the pathogenesis and treatment of AD, and the latest progress in the development of JNK3 inhibitors.

引用

页数：14

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