Intermittent fasting attenuates lipopolysaccharide-induced neuroinflammation and memory impairment.
Open accessAbstract
BACKGROUND: Systemic bacterial infections often result in enduring cognitive impairment and are a risk factor for dementia. There are currently no effective treatments for infection-induced cognitive impairment. Previous studies have shown that intermittent fasting (IF) can increase the resistance of neurons to injury and disease by stimulating adaptive cellular stress responses. However, the impact of IF on the cognitive sequelae of systemic and brain inflammation is unknown. METHODS: Rats on IF for 30 days received 1 mg/kg of lipopolysaccharide (LPS) or saline intravenously. Half of the rats were subjected to behavioral tests and the other half were euthanized two hours after LPS administration and the hippocampus was dissected and frozen for analyses. RESULTS: Here, we report that IF ameliorates cognitive deficits in a rat model of sepsis by a mechanism involving NF-κB activation, suppression of the expression of pro-inflammatory cytokines, and enhancement of neurotrophic support. Treatment of rats with LPS resulted in deficits in cognitive performance in the Barnes maze and inhibitory avoidance tests, without changing locomotor activity, that were ameliorated in rats that had been maintained on the IF diet. IF also resulted in reduced levels of mRNAs encoding the LPS receptor TLR4 and inducible nitric oxide synthase (iNOS) in the hippocampus. Moreover, IF prevented LPS-induced elevation of IL-1α, IL-1β and TNF-α levels, and prevented the LPS-induced reduction of BDNF levels in the hippocampus. IF also significantly attenuated LPS-induced elevations of serum IL-1β, IFN-γ, RANTES, TNF-α and IL-6 levels. CONCLUSIONS: Taken together, our results suggest that IF induces adaptive responses in the brain and periphery that can suppress inflammation and preserve cognitive function in an animal model of systemic bacterial infection.
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Prolonged fasting reduces inflammation, with β-HB selectively suppressing inflammasome activation in response to lipotoxic fatty acids.
“Prolonged fasting reduces inflammation, with β-HB selectively suppressing inflammasome activation in response to lipotoxic fatty acids (Vasconcelos et al., 2014).”
From Microtubule-associated protein 1 light chain 3B, (LC3B) is necessary to maintain lipid-mediated homeostasis in the retinal pigment epithelium (2018) · cites this paper as Vasconcelos et al., 2014
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- Authors
- Vasconcelos, A. R., Yshii, L. M., Viel, T. A., Buck, H. S., Mattson, M. P., Scavone, C., & Kawamoto, E. M.
- Affiliations
- Universidade de São Paulo (BR)
- Faculdade de Ciências Médicas da Santa Casa de São Paulo (BR)
- National Institute on Aging (US)
- Venue
- Journal of Neuroinflammation
- Published
- 2014-05-06
- Volume
- 11
- Issue
- 1
- Pages
- 85-85
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC4041059
- OpenAlex
- W2097170254
- Cited by
- 210
- References
- 93
- Citations by year
- 2026: 8 · 2025: 16 · 2024: 27 · 2023: 21 · 2022: 19 · 2021: 19 · 2020: 20 · 2019: 15 · 2018: 22 · 2017: 13 · 2016: 14 · 2015: 15 · 2014: 1
- FWCI
- 9.53
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (publishedVersion)
- Funders
- Fundação de Amparo à Pesquisa do Estado de São Paulo (08/58865-9, 06/57729-9, 2011.1.9333.1.3)
- Conselho Nacional de Desenvolvimento Científico e Tecnológico (2011.1.9333.1.3)
- Universidade de São Paulo (#2011.1.9333.1.3)
- National Institutes of Health
- National Institute on Aging
- Topics
- Health Sciences › Medicine › Physiology › Dietary Effects on Health
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- intermittent fasting, lipopolysaccharide, neuroinflammation, memory impairment, sepsis, NF-κB, inflammatory cytokines, TLR4, inducible nitric oxide synthase, brain-derived neurotrophic factor, hippocampus, cognitive impairment, systemic bacterial infection, dementia
- MeSH terms
- Animals, Avoidance Learning, Brain, Disease Models, Animal, Fasting, Gene Expression Regulation, Inflammation, Lipopolysaccharides, Male, Memory Disorders, Motor Activity, Psychomotor Performance, Cytokines, NF-kappa B, Rats, Wistar, Maze Learning, Electrophoretic Mobility Shift Assay, Toll-Like Receptor 4, Rats, Nitric Oxide Synthase Type II
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