CoChat
Sign Up
Cited by 26Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Microglia as a cellular target of diclofenac therapy in Alzheimer’s disease

Open access
Stopschinski, Barbara E., Weideman, Rick A., McMahan, Danni, Jacob, David A., Little, Bertis B., Chiang, Hsueh-Sheng, Saez Calveras, Nil, Stuve, Olaf·2023·Therapeutic Advances in Neurological Disorders
DOI 10.1177/17562864231156674PMC PMC9974624
Open this paper in CoChat — free account

Abstract

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1177/17562864231156674

Cites

27 of 27 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Unlike other pain-relievers, diclofenac represses the release of the inflammatory cytokine interleukin-1β and reduces activation of microglia.

    “Unlike the other pain-relievers, diclofenac represses the release of the inflammatory cytokine interleukin-1β and reduces activation of microglia (Stopschinski et al. 2023).”

    From Perineuronal net deglycosylation associates with tauopathy‐induced gliosis and neurodegeneration (2024) · cites this paper as Stopschinski et al. 2023

    In “Mechanisms of action beyond COX inhibition” (page not provided), the review reports that diclofenac had a modest effect on IL-1β release. It attributes reduced microglial activation to mefenamic acid, not diclofenac, and the reported comparison with other NSAIDs concerns fenamates rather than diclofenac. (LLM, conf=0.89)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 95

  1. [2]Mendiola-Precoma J Berumen LC Padilla K, et al. Therapies for prevention and treatment of Alzheimer’s disease. Biomed Res Int 2016; 2016: 2589276. 27547756 PMC4980501
  2. [4]Wang WY Tan MS Yu JT, et al. Role of pro-inflammatory cytokines released from microglia in Alzheimer’s disease. Ann Transl Med 2015; 3: 136. 26207229 PMC4486922
  3. [5]Jaturapatporn D Isaac MG McCleery J, et al. Aspirin, steroidal and non-steroidal anti-inflammatory drugs for the treatment of Alzheimer’s disease. Cochrane Database Syst Rev 2012; 2: CD006378. PMC11337172 22336816
  4. [6]Zhang C Wang Y Wang D, et al. NSAID exposure and risk of Alzheimer’s disease: an updated meta-analysis from cohort studies. Front Aging Neurosci 2018; 10: 83. 29643804 PMC5882872
  5. [7]Stuve O Weideman RA McMahan DM, et al. Diclofenac reduces the risk of Alzheimer’s disease: a pilot analysis of NSAIDs in two US veteran populations. Ther Adv Neurol Disord 2020; 13: 1756286420935676. 32647537 PMC7325551
  6. [8]Daniels MJ Rivers-Auty J Schilling T, et al. Fenamate NSAIDs inhibit the NLRP3 inflammasome and protect against Alzheimer’s disease in rodent models. Nat Commun 2016; 7: 12504. 27509875 PMC4987536
  7. [9]Querfurth HW LaFerla FM. Alzheimer’s disease. N Engl J Med 2010; 362: 329– 344. 20107219
  8. [10]Kametani F Hasegawa M. Reconsideration of amyloid hypothesis and tau hypothesis in Alzheimer’s disease. Front Neurosci 2018; 12: 25. 29440986 PMC5797629
  9. [11]Lue LF Kuo YM Roher AE, et al. Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer’s disease. Am J Pathol 1999; 155: 853– 862. 10487842 PMC1866907
  10. [13]Braak H Del Tredici K. Are cases with tau pathology occurring in the absence of Abeta deposits part of the AD-related pathological process? Acta Neuropathol 2014; 128: 767– 772. 25359108
  11. [14]Pascoal TA Benedet AL Ashton NJ, et al. Microglial activation and tau propagate jointly across Braak stages. Nat Med 2021; 27: 1592– 1599. 34446931
  12. [15]St-Pierre MK VanderZwaag J Loewen S, et al. All roads lead to heterogeneity: the complex involvement of astrocytes and microglia in the pathogenesis of Alzheimer’s disease. Front Cell Neurosci 2022; 16: 932572. 36035256 PMC9413962
  13. [16]Davalos D Grutzendler J Yang G, et al. ATP mediates rapid microglial response to local brain injury in vivo. Nat Neurosci 2005; 8: 752– 758. 15895084
  14. [17]Giulian D. Ameboid microglia as effectors of inflammation in the central nervous system. J Neurosci Res 1987; 18: 155–171, 132–133. 3500323
  15. [19]Krasemann S Madore C Cialic R, et al. The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases. Immunity 2017; 47: 566– 581. 28930663 PMC5719893
  16. [20]Keren-Shaul H Spinrad A Weiner A, et al. A unique microglia type associated with restricting development of Alzheimer’s Disease. Cell 2017; 169: 1276– 1290. 28602351
  17. [21]Delizannis AT Nonneman A Tsering W, et al. Effects of microglial depletion and TREM2 deficiency on Abeta plaque burden and neuritic plaque tau pathology in 5XFAD mice. Acta Neuropathol Commun 2021; 9: 150. 34503586 PMC8428059
  18. [23]Swartzlander DB Propson NE Roy ER, et al. Concurrent cell type-specific isolation and profiling of mouse brains in inflammation and Alzheimer’s disease. JCI Insight 2018; 3: e121109. PMC6124528 29997299
  19. [24]Romero-Molina C Navarro V Sanchez-Varo R, et al. Distinct microglial responses in two transgenic murine models of TAU pathology. Front Cell Neurosci 2018; 12: 421. 30487735 PMC6246744
  20. [28]Maeda J Minamihisamatsu T Shimojo M, et al. Distinct microglial response against Alzheimer’s amyloid and tau pathologies characterized by P2Y12 receptor. Brain Commun 2021; 3: fcab011. PMC7901060 33644757
  21. [30]John Lin CC Yu K Hatcher A, et al. Identification of diverse astrocyte populations and their malignant analogs. Nat Neurosci 2017; 20: 396– 405. 28166219 PMC5824716
  22. [31]Verkhratsky A Rodrigues JJ Pivoriunas A, et al. Astroglial atrophy in Alzheimer’s disease. Pflugers Arch 2019; 471: 1247– 1261. 31520182
  23. [32]Habib N McCabe C Medina S, et al. Disease-associated astrocytes in Alzheimer’s disease and aging. Nat Neurosci 2020; 23: 701– 706. 32341542 PMC9262034
  24. [33]Zhou Y Song WM Andhey PS, et al. Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer’s disease. Nat Med 2020; 26: 131– 142. 31932797 PMC6980793
  25. [35]Wolf SA Boddeke HW Kettenmann H. Microglia in physiology and disease. Annu Rev Physiol 2017; 79: 619– 643. 27959620
  26. [36]Kettenmann H Hanisch UK Noda M, et al. Physiology of microglia. Physiol Rev 2011; 91: 461– 553. 21527731
  27. [37]Heneka MT Carson MJ El Khoury J, et al. Neuroinflammation in Alzheimer’s disease. Lancet Neurol 2015; 14: 388– 405. 25792098 PMC5909703
  28. [39]Streit WJ Braak H Xue QS, et al. Dystrophic (senescent) rather than activated microglial cells are associated with tau pathology and likely precede neurodegeneration in Alzheimer’s disease. Acta Neuropathol 2009; 118: 475– 485. 19513731 PMC2737117
  29. [40]Qin Q Wang M Yin Y, et al. The specific mechanism of TREM2 regulation of synaptic clearance in Alzheimer’s disease. Front Immunol 2022; 13: 845897. 35663962 PMC9160359
  30. [43]Yoshiyama Y Higuchi M Zhang B, et al. Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse model. Neuron 2007; 53: 337– 351. 17270732
  31. [44]Hollingworth P Harold D Sims R, et al. Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer’s disease. Nat Genet 2011; 43: 429– 435. 21460840 PMC3084173
  32. [48]Mendiola AS Cardona AE. The IL-1beta phenomena in neuroinflammatory diseases. J Neural Transm 2018; 125: 781– 795. 28534174 PMC5699978
  33. [49]Cacabelos R Alvarez XA Fernández-Novoa L, et al. Brain interleukin-1 beta in Alzheimer’s disease and vascular dementia. Methods Find Exp Clin Pharmacol 1994; 16: 141– 151. 8007743
  34. [52]Griffin WS Stanley LC Ling C, et al. Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease. Proc Natl Acad Sci U S A 1989; 86: 7611– 7615. 2529544 PMC298116
  35. [53]Heneka MT Kummer MP Stutz A, et al. NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice. Nature 2013; 493: 674– 678. 23254930 PMC3812809
  36. [54]Ye L Huang Y Zhao L, et al. IL-1beta and TNF-alpha induce neurotoxicity through glutamate production: a potential role for neuronal glutaminase. J Neurochem 2013; 125: 897– 908. 23578284 PMC3747774
  37. [56]Sheng JG Zhu SG Jones RA, et al. Interleukin-1 promotes expression and phosphorylation of neurofilament and tau proteins in vivo. Exp Neurol 2000; 163: 388– 391. 10833312 PMC3886634
  38. [57]Li Y Liu L Barger SW, et al. Interleukin-1 mediates pathological effects of microglia on tau phosphorylation and on synaptophysin synthesis in cortical neurons through a p38-MAPK pathway. J Neurosci 2003; 23: 1605– 1611. 12629164 PMC3833596
  39. [60]Rouzer CA Marnett LJ. Cyclooxygenases: structural and functional insights. J Lipid Res 2009; 50(Suppl.): S29–S34. PMC2674713 18952571
  40. [61]Feng L Sun W Xia Y, et al. Cloning two isoforms of rat cyclooxygenase: differential regulation of their expression. Arch Biochem Biophys 1993; 307: 361– 368. 8274023
  41. [62]Chandrasekharan NV Dai H Roos KL, et al. COX-3, a cyclooxygenase-1 variant inhibited by acetaminophen and other analgesic/antipyretic drugs: cloning, structure, and expression. Proc Natl Acad Sci U S A 2002; 99: 13926– 13931. 12242329 PMC129799
  42. [63]Yuan C Smith WL. A cyclooxygenase-2-dependent prostaglandin E2 biosynthetic system in the Golgi apparatus. J Biol Chem 2015; 290: 5606– 5620. 25548276 PMC4342474
  43. [64]Kitamura Y Shimohama S Koike H, et al. Increased expression of cyclooxygenases and peroxisome proliferator-activated receptor-gamma in Alzheimer’s disease brains. Biochem Biophys Res Commun 1999; 254: 582– 586. 9920782
  44. [65]Deininger MH Schluesener HJ. Cyclooxygenases-1 and -2 are differentially localized to microglia and endothelium in rat EAE and glioma. J Neuroimmunol 1999; 95: 202– 208. 10229132
  45. [66]Yamagata K Andreasson KI Kaufmann WE, et al. Expression of a mitogen-inducible cyclooxygenase in brain neurons: regulation by synaptic activity and glucocorticoids. Neuron 1993; 11: 371– 386. 8352945
  46. [67]Choi SH Langenbach R Bosetti F. Genetic deletion or pharmacological inhibition of cyclooxygenase-1 attenuate lipopolysaccharide-induced inflammatory response and brain injury. FASEB J 2008; 22: 1491– 1501. 18162486 PMC2386977
  47. [68]Aid S Langenbach R Bosetti F. Neuroinflammatory response to lipopolysaccharide is exacerbated in mice genetically deficient in cyclooxygenase-2. J Neuroinflammation 2008; 5: 17. 18489773 PMC2409311
  48. [69]Wang P Guan PP Wang T, et al. Aggravation of Alzheimer’s disease due to the COX-2-mediated reciprocal regulation of IL-1beta and Abeta between glial and neuron cells. Aging Cell 2014; 13: 605– 615. 24621265 PMC4326948
  49. [70]Choi SH Bosetti F. Cyclooxygenase-1 null mice show reduced neuroinflammation in response to beta-amyloid. Aging 2009; 1: 234– 244. 20157512 PMC2806008
  50. [71]Mhillaj E Morgese MG Tucci P, et al. Celecoxib prevents cognitive impairment and neuroinflammation in soluble amyloid beta-treated rats. Neuroscience 2018; 372: 58– 73. 29306052
  51. [72]Xiang Z Ho L Yemul S, et al. Cyclooxygenase-2 promotes amyloid plaque deposition in a mouse model of Alzheimer’s disease neuropathology. Gene Expr 2002; 10: 271– 278. 12450219 PMC5977525
  52. [73]Hoozemans JJ Rozemuller JM van Haastert ES, et al. Cyclooxygenase-1 and -2 in the different stages of Alzheimer’s disease pathology. Curr Pharm Des 2008; 14: 1419– 1427. 18537664
  53. [74]Hoozemans JJ Rozemuller AJ Janssen I, et al. Cyclooxygenase expression in microglia and neurons in Alzheimer’s disease and control brain. Acta Neuropathol 2001; 101: 2– 8. 11194936
  54. [75]Yermakova AV Rollins J Callahan LM, et al. Cyclooxygenase-1 in human Alzheimer and control brain: quantitative analysis of expression by microglia and CA3 hippocampal neurons. J Neuropathol Exp Neurol 1999; 58: 1135– 1146. 10560656
  55. [76]Ohnishi A Senda M Yamane T, et al. Exploratory human PET study of the effectiveness of (11)C-ketoprofen methyl ester, a potential biomarker of neuroinflammatory processes in Alzheimer’s disease. Nucl Med Biol 2016; 43: 438– 444. 27183464
  56. [77]Bettcher BM Tansey MG Dorothee G, et al. Peripheral and central immune system crosstalk in Alzheimer disease – a research prospectus. Nat Rev Neurol 2021; 17: 689– 701. 34522039 PMC8439173
  57. [78]Sipilä PN Heikkilä N Lindbohm JV, et al. Hospital-treated infectious diseases and the risk of dementia: a large, multicohort, observational study with a replication cohort. Lancet Infect Dis 2021; 21: 1557– 1567. 34166620 PMC8592915
  58. [80]Cattaneo A Cattane N Galluzzi S, et al. Association of brain amyloidosis with pro-inflammatory gut bacterial taxa and peripheral inflammation markers in cognitively impaired elderly. Neurobiol Aging 2017; 49: 60– 68. 27776263
  59. [82]Liu YJ Guo DW Tian L, et al. Peripheral T cells derived from Alzheimer’s disease patients overexpress CXCR2 contributing to its transendothelial migration, which is microglial TNF-alpha-dependent. Neurobiol Aging 2010; 31: 175– 188. 18462836
  60. [83]Saresella M La Rosa F Piancone F, et al. The NLRP3 and NLRP1 inflammasomes are activated in Alzheimer’s disease. Mol Neurodegener 2016; 11: 23. 26939933 PMC4778358
  61. [84]Tejera D Mercan D Sanchez-Caro JM, et al. Systemic inflammation impairs microglial Abeta clearance through NLRP3 inflammasome. EMBO J 2019; 38: e101064. PMC6717897 31359456
  62. [85]Beyer MMS Lonnemann N Remus A, et al. Enduring changes in neuronal function upon systemic inflammation are NLRP3 inflammasome dependent. J Neurosci 2020; 40: 5480– 5494. 32499379 PMC7343321
  63. [86]Teeling JL Cunningham C Newman TA, et al. The effect of non-steroidal anti-inflammatory agents on behavioural changes and cytokine production following systemic inflammation: implications for a role of COX-1. Brain Behav Immun 2010; 24: 409– 419. 19931610 PMC3098384
  64. [87]Wyss-Coray T. Inflammation in Alzheimer disease: driving force, bystander or beneficial response? Nat Med 2006; 12: 1005– 1015. 16960575
  65. [88]Ghlichloo I Gerriets V. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs). Treasure Island, FL: StatPearls, 2022. 31613522
  66. [89]Vane JR. Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nat New Biol 1971; 231: 232– 235. 5284360
  67. [90]Vlad SC Miller DR Kowall NW, et al. Protective effects of NSAIDs on the development of Alzheimer disease. Neurology 2008; 70: 1672– 1677. 18458226 PMC2758242
  68. [91]Rivers-Auty J Mather AE Peters R, et al. Anti-inflammatories in Alzheimer’s disease-potential therapy or spurious correlate? Brain Commun 2020; 2: fcaa109. PMC7585697 33134914
  69. [92]Rogers J Kirby LC Hempelman SR, et al. Clinical trial of indomethacin in Alzheimer’s disease. Neurology 1993; 43: 1609– 1611. 8351023
  70. [94]Aisen PS Schafer KA Grundman M, et al. Effects of rofecoxib or naproxen vs placebo on Alzheimer disease progression: a randomized controlled trial. JAMA 2003; 289: 2819– 2826. 12783912
  71. [95]Aisen PS Schmeidler J Pasinetti GM. Randomized pilot study of nimesulide treatment in Alzheimer’s disease. Neurology 2002; 58: 1050– 1054. 11940691
  72. [96]Reines SA Block GA Morris JC, et al. Rofecoxib: no effect on Alzheimer’s disease in a 1-year, randomized, blinded, controlled study. Neurology 2004; 62: 66– 71. 14718699
  73. [97]Soininen H West C Robbins J, et al. Long-term efficacy and safety of celecoxib in Alzheimer’s disease. Dement Geriatr Cogn Disord 2007; 23: 8– 21. 17068392
  74. [100]ADAPT-FS Research Group. Follow-up evaluation of cognitive function in the randomized Alzheimer’s disease anti-inflammatory prevention trial and its follow-up study. Alzheimers Dement 2015; 11: 216– 225. 25022541 PMC4287453
  75. [101]Landi F Cesari M Onder G, et al. Non-steroidal anti-inflammatory drug (NSAID) use and Alzheimer disease in community-dwelling elderly patients. Am J Geriatr Psychiatry 2003; 11: 179– 185. 12611747
  76. [102]Scharf S Mander A Ugoni A, et al. A double-blind, placebo-controlled trial of diclofenac/misoprostol in Alzheimer’s disease. Neurology 1999; 53: 197– 201. 10408559
  77. [103]Altman R Bosch B Brune K, et al. Advances in NSAID development: evolution of diclofenac products using pharmaceutical technology. Drugs 2015; 75: 859– 877. 25963327 PMC4445819
  78. [104]Amanullah A Upadhyay A Dhiman R, et al. Development and challenges of diclofenac-based novel therapeutics: targeting cancer and complex diseases. Cancers 2022; 14: 4385. 36139546 PMC9496891
  79. [105]Fukuda M Kitaichi K Abe F, et al. Altered brain penetration of diclofenac and mefenamic acid, but not acetaminophen, in Shiga-like toxin II-treated mice. J Pharmacol Sci 2005; 97: 525– 532. 15821337
  80. [106]Menassé R Hedwall PR Kraetz J, et al. Pharmacological properties of diclofenac sodium and its metabolites. Scand J Rheumatol Suppl 1978; 22: 5– 16. 98835
  81. [107]Zecca L Ferrario P Costi P. Determination of diclofenac and its metabolites in plasma and cerebrospinal fluid by high-performance liquid chromatography with electrochemical detection. J Chromatogr 1991; 567: 425– 432. 1939474
  82. [108]Kokki H Kumpulainen E Laisalmi M, et al. Diclofenac readily penetrates the cerebrospinal fluid in children. Br J Clin Pharmacol 2008; 65: 879– 884. 18477264 PMC2485236
  83. [109]Joo Y Kim HS Woo RS, et al. Mefenamic acid shows neuroprotective effects and improves cognitive impairment in vitro and in vivo Alzheimer’s disease models. Mol Pharmacol 2006; 69: 76– 84. 16223958
  84. [110]Lam J Wulff H. The lymphocyte potassium channels Kv1.3 and KCa3.1 as targets for immunosuppression. Drug Dev Res 2011; 72: 573– 584. 22241939 PMC3253536
  85. [111]Peretz A Degani N Nachman R, et al. Meclofenamic acid and diclofenac, novel templates of KCNQ2/Q3 potassium channel openers, depress cortical neuron activity and exhibit anticonvulsant properties. Mol Pharmacol 2005; 67: 1053– 1066. 15598972
  86. [112]Maezawa I Nguyen HM Di Lucente J, et al. Kv1.3 inhibition as a potential microglia-targeted therapy for Alzheimer’s disease: preclinical proof of concept. Brain 2018; 141: 596– 612. 29272333 PMC5837198
  87. [113]Hirohata M Ono K Naiki H, et al. Non-steroidal anti-inflammatory drugs have anti-amyloidogenic effects for Alzheimer’s beta-amyloid fibrils in vitro. Neuropharmacology 2005; 49: 1088– 1099. 16125740
  88. [115]Adwan L Subaiea GM Basha R, et al. Tolfenamic acid reduces tau and CDK5 levels: implications for dementia and tauopathies. J Neurochem 2015; 133: 266– 272. 25279694 PMC4385008
  89. [116]Adwan L Subaiea GM Zawia NH. Tolfenamic acid downregulates BACE1 and protects against lead-induced upregulation of Alzheimer’s disease related biomarkers. Neuropharmacology 2014; 79: 596– 602. 24462621 PMC7057722
  90. [117]Leso A Bihaqi SW Masoud A, et al. Loss in efficacy measures of tolfenamic acid in a tau knock-out model: relevance to Alzheimer’s disease. Exp Biol Med 2019; 244: 1062– 1069. PMC6775567 31450960
  91. [118]Abdelrahim M Baker CH Abbruzzese JL, et al. Tolfenamic acid and pancreatic cancer growth, angiogenesis, and Sp protein degradation. J Natl Cancer Inst 2006; 98: 855– 868. 16788159
  92. [119]Chang R Yee KL Sumbria RK. Tumor necrosis factor alpha Inhibition for Alzheimer’s Disease. J Cent Nerv Syst Dis 2017; 9: 1179573517709278. 28579870 PMC5436834
  93. [120]Li L Rossoni G Sparatore A, et al. Anti-inflammatory and gastrointestinal effects of a novel diclofenac derivative. Free Radic Biol Med 2007; 42: 706– 719. 17291994
  94. [121]Vieira V Glassmann D Marafon P, et al. Effect of diclofenac sodium on seizures and inflammatory profile induced by kindling seizure model. Epilepsy Res 2016; 127: 107– 113. 27589413
  95. [122]Hill J Zawia NH. Fenamates as potential therapeutics for neurodegenerative disorders. Cells 2021; 10: 702. 33809987 PMC8004804

Cited by

Sorted by citations

Authors
Stopschinski, B. E., Weideman, R. A., McMahan, D., Jacob, D. A., Little, B. B., Chiang, H.-S., Saez Calveras, N., & Stuve, O.
Affiliations
  • The University of Texas Southwestern Medical Center (US)
  • Dallas VA Medical Center (US)
  • VA Heart of Texas Health Care Network (US)
  • University of Louisville (US)
  • Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX, USA
ORCID
Venue
Therapeutic Advances in Neurological Disorders
Publisher
SAGE Publications
Published
2023-01
Volume
16
Pages
17562864231156674-17562864231156674
ISSN
  • 1756-2856 (ISSN-L)
  • 1756-2864
DOI
10.1177/17562864231156674
PMC
PMC9974624
OpenAlex
W4323286837
Cited by
26
References
27
Citations by year
2026: 3 · 2025: 10 · 2024: 11 · 2023: 2
FWCI
0.93
Type
journal article
Language
en
Open access
Licence
Locations
  • Therapeutic Advances in Neurological Disorders (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
diclofenac, Alzheimer's disease, microglia, nonsteroidal anti-inflammatory drugs, fenamates, neuroinflammation, amyloid plaques, neurofibrillary tangles, anti-inflammatory therapy

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review