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Through KP, L-tryptophan is catabolized into neurotoxic and neuroprotective metabolites. The overactivation of indolamine 2,3-dioxygenase1 (IDO1), the first rate-limiting enzyme of KP, and the abnormal accumulation of KP metabolites have been noted in AD, and blocking IDO1 has been suggested as a therapeutic strategy. However, the expression patterns of KP enzymes in AD, and whether these enzymes are related to AD pathogenesis, have not been fully studied. Herein, we examined the expression patterns of inflammatory cytokines, neurotrophic factors and KP enzymes, and the activity of IDO1 and IDO1 effector pathway AhR (aryl hydrocarbon receptor) in AD mice. We studied the effects of IDO1 inhibitors on A\u03b2-related neuroinflammation in rat primary neurons, mouse hippocampal neuronal cells, and APP\/PS1 mice. The results further demonstrated the importance of IDO1-catalyzed KP in neuroinflammation in Alzheimer\u2019s disease.<\/jats:p>","DOI":"10.1177\/15333175231214861","type":"journal-article","created":{"date-parts":[[2023,11,9]],"date-time":"2023-11-09T15:22:08Z","timestamp":1699543328000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":20,"title":["The Protective Effect of IDO1 Inhibition in A\u03b2-Treated Neurons and APP\/PS1 Mice"],"prefix":"10.1177","volume":"38","author":[{"given":"Zhenzhen","family":"Duan","sequence":"first","affiliation":[{"name":"School of Life Sciences, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Shi","sequence":"additional","affiliation":[{"name":"School of Life Sciences, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, 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