Microglia as a cellular target of diclofenac therapy in Alzheimer’s disease
Alzheimer’s disease (AD) is an untreatable cause of dementia, and new therapeutic approaches are urgently needed. AD pathology is defined by extracellular amyloid plaques and intracellular neurofibrillary tangles. Research of the past decades has suggested that neuroinflammation plays a critical rol...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
SAGE Publishing
2023-02-01
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| Series: | Therapeutic Advances in Neurological Disorders |
| Online Access: | https://doi.org/10.1177/17562864231156674 |
| _version_ | 1797893470985125888 |
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| author | Barbara E. Stopschinski Rick A. Weideman Danni McMahan David A. Jacob Bertis B. Little Hsueh-Sheng Chiang Nil Saez Calveras Olaf Stuve |
| author_facet | Barbara E. Stopschinski Rick A. Weideman Danni McMahan David A. Jacob Bertis B. Little Hsueh-Sheng Chiang Nil Saez Calveras Olaf Stuve |
| author_sort | Barbara E. Stopschinski |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) is an untreatable cause of dementia, and new therapeutic approaches are urgently needed. AD pathology is defined by extracellular amyloid plaques and intracellular neurofibrillary tangles. 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. |
| first_indexed | 2024-04-10T06:53:23Z |
| format | Article |
| id | doaj.art-ed394128eb9149f986db48d541441288 |
| institution | Directory Open Access Journal |
| issn | 1756-2864 |
| language | English |
| last_indexed | 2024-04-10T06:53:23Z |
| publishDate | 2023-02-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Therapeutic Advances in Neurological Disorders |
| spelling | doaj.art-ed394128eb9149f986db48d5414412882023-02-28T08:03:52ZengSAGE PublishingTherapeutic Advances in Neurological Disorders1756-28642023-02-011610.1177/17562864231156674Microglia as a cellular target of diclofenac therapy in Alzheimer’s diseaseBarbara E. StopschinskiRick A. WeidemanDanni McMahanDavid A. JacobBertis B. LittleHsueh-Sheng ChiangNil Saez CalverasOlaf StuveAlzheimer’s disease (AD) is an untreatable cause of dementia, and new therapeutic approaches are urgently needed. AD pathology is defined by extracellular amyloid plaques and intracellular neurofibrillary tangles. 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.https://doi.org/10.1177/17562864231156674 |
| spellingShingle | Barbara E. Stopschinski Rick A. Weideman Danni McMahan David A. Jacob Bertis B. Little Hsueh-Sheng Chiang Nil Saez Calveras Olaf Stuve Microglia as a cellular target of diclofenac therapy in Alzheimer’s disease Therapeutic Advances in Neurological Disorders |
| title | Microglia as a cellular target of diclofenac therapy in Alzheimer’s disease |
| title_full | Microglia as a cellular target of diclofenac therapy in Alzheimer’s disease |
| title_fullStr | Microglia as a cellular target of diclofenac therapy in Alzheimer’s disease |
| title_full_unstemmed | Microglia as a cellular target of diclofenac therapy in Alzheimer’s disease |
| title_short | Microglia as a cellular target of diclofenac therapy in Alzheimer’s disease |
| title_sort | microglia as a cellular target of diclofenac therapy in alzheimer s disease |
| url | https://doi.org/10.1177/17562864231156674 |
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