Lee Jong Kil, Kim Nam-Jung
Department of Pharmacy, College of Pharmacy, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea.
Molecules. 2017 Aug 2;22(8):1287. doi: 10.3390/molecules22081287.
P38 mitogen-activated protein kinase (MAPK) is a crucial target for chronic inflammatory diseases. Alzheimer's disease (AD) is characterized by the presence of amyloid plaques and neurofibrillary tangles in the brain, as well as neurodegeneration, and there is no known cure. Recent studies on the underlying biology of AD in cellular and animal models have indicated that p38 MAPK is capable of orchestrating diverse events related to AD, such as tau phosphorylation, neurotoxicity, neuroinflammation and synaptic dysfunction. Thus, the inhibition of p38 MAPK is considered a promising strategy for the treatment of AD. In this review, we summarize recent advances in the targeting of p38 MAPK as a potential strategy for the treatment of AD and envision possibilities of p38 MAPK inhibitors as a fundamental therapeutics for AD.
P38丝裂原活化蛋白激酶（MAPK）是慢性炎症性疾病的关键靶点。阿尔茨海默病（AD）的特征是大脑中存在淀粉样斑块和神经原纤维缠结，以及神经退行性变，且尚无已知的治愈方法。最近在细胞和动物模型中对AD潜在生物学机制的研究表明，p38 MAPK能够协调与AD相关的各种事件，如tau蛋白磷酸化、神经毒性、神经炎症和突触功能障碍。因此，抑制p38 MAPK被认为是治疗AD的一种有前景的策略。在这篇综述中，我们总结了将p38 MAPK作为AD潜在治疗策略的最新进展，并展望了p38 MAPK抑制剂作为AD基本治疗药物的可能性。
