期刊
FASEB JOURNAL
卷 33, 期 1, 页码 13-33出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.201800355RRRR
关键词
prostaglandins; neuroinflammation; apoptosis; autophagy; synaptic plasticity
资金
- National Natural Science Foundation of China [31571064, 81771167, 81500934]
- Fundamental Research Foundation of Northeastern University (Shenyang, China) [N172008008, N172004005]
Elevated levels of cyclooxygenase-2 (COX-2) and prostaglandins (PGs) are involved in the pathogenesis of Alzheimer's disease (AD), which is characterized by the accumulation of -amyloid protein (A) and tau hyperphosphorylation. However, the gaps in our knowledge of the roles of COX-2 and PGs in AD have not been filled. Here, we summarized the literature showing that COX-2 dysregulation obviously influences abnormal cleavage of -amyloid precursor protein, aggregation and deposition of A in -amyloid plaques and the inclusion of phosphorylated tau in neurofibrillary tangles. Neuroinflammation, oxidative stress, synaptic plasticity, neurotoxicity, autophagy, and apoptosis have been assessed to elucidate the mechanisms of COX-2 regulation of AD. Notably, an imbalance of these factors ultimately produces cognitive decline. The current review substantiates our understanding of the mechanisms of COX-2-induced AD and establishes foundations for the design of feasible therapeutic strategies to treat AD.Guan, P.-P., Wang, P. Integrated communications between cyclooxygenase-2 and Alzheimer's disease.
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