Anti-Inflammatory Drug Therapy Alters β-Amyloid Processing and Deposition in an Animal Model of Alzheimer's Disease
Open accessAbstract
Alzheimer's disease (AD) is characterized by a microglial-mediated inflammatory response elicited by extensive amyloid deposition in the brain. Nonsteroidal anti-inflammatory drug (NSAID) treatment reduces AD risk, slows disease progression, and reduces microglial activation; however, the basis of these effects is unknown. We report that treatment of 11-month-old Tg2576 mice overexpressing human amyloid precursor protein (APP) with the NSAID ibuprofen for 16 weeks resulted in the dramatic and selective reduction of SDS-soluble β-amyloid (Aβ)42, whereas it had smaller effects on SDS-soluble Aβ 40 levels. Ibuprofen treatment resulted in 60% reduction of amyloid plaque load in the cortex of these animals.In vitro studies using APP-expressing 293 cells showed that ibuprofen directly affected APP processing, specifically reducing the production of Aβ 42. Ibuprofen treatment resulted in a significant reduction in microglial activation in the Tg2576 mice, as measured by CD45 and CD11b expression. NSAIDs activate the nuclear hormone receptor peroxisome proliferator-activated receptor γ (PPARγ); however, a potent agonist of this receptor, pioglitazone, only modestly reduced SDS-soluble Aβ levels and did not affect amyloid plaque burden or microglia activation, indicating that PPARγ activation is not involved in the Aβ lowering effect of NSAIDs. These data show that chronic NSAID treatment can reduce brain Aβ levels, amyloid plaque burden, and microglial activation in an animal model of Alzheimer's disease.
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Sustained PPARγ or LXR activation results in amelioration of AD-related pathophysiology in AD mouse models.
“Sustained PPARγ or LXR activation results in amelioration of AD-related pathophysiology in AD mouse models (Yan et al., 2003; Pedersen and Flynn, 2004; Heneka et al., 2005; Koldamova et al., 2005a; Riddell et al., 2007; Zelcer et al., 2007; Jiang et al., 2008; Donkin et al., 2010; Fitz et al., 2010; Toledo and Inestrosa, 2010).”
From Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease (2012) · cites this paper as Yan et al., 2003
The Results report that four months of treatment with the PPARγ agonist pioglitazone significantly reduced SDS-soluble Aβ40 in Tg2576 mice. The Introduction and Discussion say it did not significantly reduce plaque burden or microglial activation, so the broader claim of ameliorated AD-related pathology overstates this study. The paper does not assess LXR activation; page numbers were not provided for these passages. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPPARγ agonists have been shown to lower soluble Aβ levels, reduce plaque burden, and improve behavior in some AD mouse models.
“Indeed, PPARγ agonists have been shown to effectively lower both soluble levels of Aβ, reduce plaque burden, and improve behavior in some AD mouse models”
From Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease (2012) · cites this paper as Yan et al., 2003
The Results report that pioglitazone significantly lowered SDS-soluble Aβ40 in Tg2576 mice, supporting the soluble-Aβ portion. The same Results say pioglitazone produced no significant change in plaque burden; the reported plaque reduction was with ibuprofen. The paper does not report behavioral improvement. (LLM, conf=0.88)
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- Authors
- Yan, Q., Zhang, J., Liu, H., Babu-Khan, S., Vassar, R., Biere, A. L., Citron, M., & Landreth, G.
- Affiliations
- Amgen (United States) (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2003-08-20
- Volume
- 23
- Issue
- 20
- Pages
- 7504-7509
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6740758
- OpenAlex
- W1678111194
- Cited by
- 469
- References
- 7
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 10 · 2023: 11 · 2022: 16 · 2021: 13 · 2020: 13 · 2019: 16 · 2018: 14 · 2017: 22 · 2016: 21 · 2015: 25 · 2014: 29 · 2013: 22 · 2012: 26
- FWCI
- 18.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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
- Alzheimer's disease, ibuprofen, nonsteroidal anti-inflammatory drugs, amyloid-beta, amyloid-beta 42, amyloid plaques, microglial activation, APP processing, Tg2576 mice, PPARγ, pioglitazone, neuroinflammation
- MeSH terms
- Pioglitazone, Alzheimer Disease, Animals, Anti-Inflammatory Agents, Non-Steroidal, Cell Line, Humans, Ibuprofen, Mice, Transgenic, Peptide Fragments, Thiazoles, Transcription Factors, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Microglia, Receptors, Cytoplasmic and Nuclear, Thiazolidinediones, Mice
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