Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease
Abstract
The hypothesis that inflammation and beta amyloid deposition are causally linked in Alzheimer's disease (AD) was tested in a transgenic mouse model. Untreated beta amyloid plaque-bearing Tg2576 mice did not differ from wild type animals in brain levels of most inflammatory mediators. Indomethacin treatment suppressed brain levels of prostaglandins by 90%, but reduced hippocampal beta amyloid by only 20%, with no effect on cortical beta amyloid. The discordant effects on beta amyloid and cyclooxygenase (COX) suggest that these effects of nonsteroidal anti-inflammatory drugs (NSAIDs) are not causally linked. Further evidence against a causal relationship is seen in an unexpected trend to lower levels of beta amyloid after an inflammatory stimulus [lipopolysaccharide (LPS)].
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IL1β overexpression enhances Aβ clearance.
“previous studies demonstrated that IL1 overexpression enhances A clearance.9,53”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [53]
Overexpression of IL1β, an inflammatory cytokine, leads to reduced Aβ pathology in mouse models of AD.
“Recent studies demonstrated that overexpression of IL1, an inflammatory cytokine leads to reduced A pathology in mouse models of AD. 9,53”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [53]
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References 44 · Cited by 102
- Authors
- Quinn, J.
- Affiliations
- Oregon Health & Science University (US)
- Corresponding author
- Quinn, J
- ORCID
- Quinn, J
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2003-04
- Volume
- 137
- Issue
- 1-2
- Pages
- 32-41
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W2159781448
- Cited by
- 102
- References
- 44
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 2 · 2016: 3 · 2015: 4 · 2014: 2 · 2013: 4 · 2012: 6
- FWCI
- 4.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- National Institute on Aging (AG 00774, AG 08017, AG 16835, AG07424, P30AG008017, R01AG016835)
- National Center for Complementary and Integrative Health (AT00066-01)
- 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, cerebral amyloidosis, amyloid-beta, neuroinflammation, Tg2576 mice, indomethacin, nonsteroidal anti-inflammatory drugs, cyclooxygenase, prostaglandins, lipopolysaccharide, hippocampus, cortical amyloid, amyloid plaques
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Anti-Inflammatory Agents, Non-Steroidal, Cerebral Cortex, Disease Models, Animal, Female, Hippocampus, Inflammation, Lipopolysaccharides, Mice, Inbred C57BL, Mice, Transgenic, Cytokines, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Mice
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