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Research of the past decades has suggested that neuroinflammation plays a critical role in the pathophysiology of AD. This has led to the idea that anti-inflammatory treatments might be beneficial. Early studies investigated non-steroidal anti-inflammatory drugs (NSAIDS) such as indomethacin, celecoxib, ibuprofen, and naproxen, which had no benefit. More recently, protective effects of diclofenac and NSAIDs in the fenamate group have been reported. Diclofenac decreased the frequency of AD significantly compared to other NSAIDs in a large retrospective cohort study. Diclofenac and fenamates share similar chemical structures, and evidence from cell and mouse models suggests that they inhibit the release of pro-inflammatory mediators from microglia with leads to the reduction of AD pathology. Here, we review the potential role of diclofenac and NSAIDs in the fenamate group for targeting AD pathology with a focus on its potential effects on microglia. <\/jats:p>","DOI":"10.1177\/17562864231156674","type":"journal-article","created":{"date-parts":[[2023,3,5]],"date-time":"2023-03-05T05:31:11Z","timestamp":1677994271000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":26,"title":["Microglia as a cellular target of diclofenac therapy in Alzheimer\u2019s disease"],"prefix":"10.1177","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5715-4567","authenticated-orcid":false,"given":"Barbara E.","family":"Stopschinski","sequence":"first","affiliation":[{"name":"Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX, USA"},{"name":"Center for Alzheimer\u2019s and Neurodegenerative Diseases, University of Texas Southwestern Medical Center, Dallas, TX, 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