高磷酸化
激酶
痴呆
发病机制
神经科学
DYRK1A型
阿尔茨海默病
化学
疾病
基因亚型
淀粉样β
细胞生物学
生物化学
医学
病理
生物
基因
作者
Pengxia Qin,Yingying Ran,Yujing Liu,Chao Wei,Xiaoyi Luan,Haoqian Niu,Jie Peng,Jie Sun,Jingde Wu
标识
DOI:10.1016/j.bioorg.2022.106090
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 Aβ amyloid plaques and neurofibrillary tangles caused by Tau hyperphosphorylation. JNK3 is involved in forming amyloid Aβ 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.
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