Journal
BIOORGANIC CHEMISTRY
Volume 128, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bioorg.2022.106090
Keywords
JNK3 inhibitors; Alzheimer?s disease; A?; Tau; Inflammation; Structure -activity relationship
Funding
- Natural Science Foundation of Shan- dong province, China [ZR2019MB017]
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This review discusses the roles of JNK3 in the pathogenesis and treatment of AD, as well as the latest progress in the development of JNK3 inhibitors.
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.
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