Amyloid Beta Pathology Exacerbates Weight Loss and Brain Cytokine Responses following Low-Dose Lipopolysaccharide in Aged Female Tg2576 Mice
Open accessAbstract
Systemic inflammation has been implicated in the progression of Alzheimer’s disease (AD); however, less is understood about how existing AD pathology contributes to adverse outcomes following acute inflammatory insults. In the present study, our goal was to determine how AD-associated amyloid beta (Aβ) pathology influences the acute neuroinflammatory and behavioral responses to a moderate systemic inflammatory insult. We treated 16–18-month-old female Tg2576 (Tg) mice, which overproduce human Aβ and develop plaques, and age-matched wild-type (WT) littermate mice with an intraperitoneal injection of 0.33 mg/kg lipopolysaccharide (LPS) or saline. Mice were then evaluated over the next 28 h for sickness/depressive-like behaviors (food intake, weight loss, locomotion, and sucrose preference), systemic inflammation (serum amyloid A, SAA), blood-brain barrier (BBB) disruption, astrogliosis (glial fibrillary acidic protein/GFAP), Aβ, and cytokine levels in the brain. We found that LPS caused a larger reduction in body weight in Tg vs. WT mice, but that other behavioral responses to LPS did not differ by genotype. BBB disruption was not apparent in either genotype following LPS. Concentrations of the systemic inflammatory marker, SAA, in the blood and brain were significantly increased with LPS but did not significantly differ by genotype. GFAP was increased in Tg mice vs. WT but was not significantly affected by LPS in either genotype. Finally, LPS-induced increases of eight cytokines (IL-1β, IL-6, IL-12 (p40), IL-10, IL-17A, MIP-1α/CCL3, MIP-1β/CCL4, and RANTES/CCL5) were found to be significantly higher in Tg mice vs. WT. In summary, our data show that Aβ pathology exacerbates the neuroinflammatory response to LPS and identifies cytokines that are selectively regulated by Aβ. The association of worse neuroinflammation with greater weight loss in Tg mice suggests that Aβ pathology could contribute to poor outcomes following a systemic inflammatory insult.
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Nonspecific microglia activation induced by lipopolysaccharide does not have the same amyloid-promoting effect as myelin dysfunction, as increases, decreases or no changes in amyloid burden have been reported.
“However, nonspecific microglia activation induced by lipopolysaccharide does not have the same amyloid-promoting effect as myelin dysfunction, as increases, decreases or no changes in amyloid burden have been reported48–51.”
From Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease (2023) · cites this paper as [51]
Results §2.4 (page unavailable) reports no significant effect of low-dose LPS on soluble or insoluble brain Aβ in the mice studied. That supports the 'no changes' example, but this paper does not report LPS-induced increases or decreases in amyloid burden or compare LPS with myelin dysfunction. Its finding is also limited to the acute treatment studied. (LLM, conf=0.86)
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- Authors
- Knopp, R. C., Baumann, K. K., Wilson, M. L., Banks, W. A., & Erickson, M. A.
- Affiliations
- University of Washington (US)
- VA Puget Sound Health Care System (US)
- Corresponding author
- Erickson, Michelle A.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2022-02-21
- Volume
- 23
- Issue
- 4
- Pages
- 2377
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC8879430
- OpenAlex
- W4213102645
- Cited by
- 17
- References
- 58
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 6 · 2023: 3 · 2022: 3
- FWCI
- 1.23
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (P50 AG005136, T32AG066574)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- amyloid-beta, Alzheimer's disease, lipopolysaccharide, neuroinflammation, weight loss, sickness behavior, systemic inflammation, Tg2576 mice, serum amyloid A, blood-brain barrier, astrocyte activation, glial fibrillary acidic protein, brain cytokines, chemokines
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Female, Gliosis, Hippocampus, Inflammation, Lipopolysaccharides, Mice, Transgenic, Weight Loss, Cytokines, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Microglia, Mice, Plaque, Amyloid
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