Central and systemic IL-1 exacerbates neurodegeneration and motor symptoms in a model of Parkinson’s disease
Open accessAbstract
Parkinson's disease is a neurodegenerative disorder with uncertain aetiology and ill-defined pathophysiology. Activated microglial cells in the substantia nigra (SN) are found in all animal models of Parkinson's disease and patients with the illness. Microglia may, however, have detrimental and protective functions in this disease. In this study, we tested the hypothesis that a sub-toxic dose of an inflammogen (lipopolysaccharide) can shift microglia to a pro-inflammatory state and exacerbate disease progression in an animal model of Parkinson's disease. Central lipopolysaccharide injection in a degenerating SN exacerbated neurodegeneration, accelerated and increased motor signs and shifted microglial activation towards a pro-inflammatory phenotype with increased interleukin-1beta (IL-1beta) secretion. Glucocorticoid treatment and specific IL-1 inhibition reversed these effects. Importantly, chronic systemic expression of IL-1 also exacerbated neurodegeneration and microglial activation in the SN. In vitro, IL-1 directly exacerbated 6-OHDA-triggered dopaminergic toxicity. In vivo, we found that nitric oxide was a downstream molecule of IL-1 action and partially responsible for the exacerbation of neurodegeneration observed. Thus, IL-1 exerts its exacerbating effect on degenerating dopaminergic neurons by direct and indirect mechanisms. This work demonstrates an unequivocal association between IL-1 overproduction and increased disease progression, pointing to inflammation as a risk factor for Parkinson's disease and suggesting that inflammation should be efficiently handled in patients to slow disease progression.
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In a different PD mouse model, blocking IL-1β signaling using an IL-1 receptor antagonist significantly attenuated neurodegeneration.
“In a different PD mouse model, blocking IL-1β signaling using an IL-1 receptor antagonist also significantly attenuated neurodegeneration.362,363”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [363]
The Results section (Fig. 5A; page not provided) reports that IL-1 receptor antagonist treatment significantly preserved dopaminergic neurons in the 6-OHDA/LPS model. However, the Fig. 1 description identifies the animals in that experiment as rats, not mice. (LLM, conf=0.93)
Experimental — accuracy not yet measuredStudies on experimental PD models argue that dopamine neurons are very susceptible to both oxidative stress and inflammation.
“Studies on experimental PD models argue that dopamine neurons are very susceptible to both oxidative stress and inflammation [121,122],”
From Beneficial Effects of Spirulina Consumption on Brain Health (2022) · cites this paper as [122]
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- Authors
- Pott Godoy, M. C., Tarelli, R., Ferrari, C. C., Sarchi, M. I., & Pitossi, F. J.
- Affiliations
- Consejo Nacional de Investigaciones Científicas y Técnicas (AR)
- Corresponding author
- Pitossi, F. J.
- ORCID
- Pitossi, F. J.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-05-26
- Volume
- 131
- Issue
- 7
- Pages
- 1880-1894
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC2442423
- OpenAlex
- W2149298826
- Cited by
- 335
- References
- 53
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 14 · 2023: 18 · 2022: 17 · 2021: 24 · 2020: 20 · 2019: 18 · 2018: 19 · 2017: 23 · 2016: 12 · 2015: 22 · 2014: 23 · 2013: 19 · 2012: 21
- FWCI
- 14.88
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Brain (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Americanae (AECID Library) (submittedVersion, cc-by-nc)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc)
- Funders
- Michael J. Fox Foundation for Parkinson's Research
- Consejo Nacional de Investigaciones Científicas y Técnicas
- Fundación YPF
- Agencia Nacional de Promoción Científica y Tecnológica (CONICET)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, IL-1β, neuroinflammation, microglial activation, substantia nigra, lipopolysaccharide, dopaminergic neuron loss, 6-hydroxydopamine, nitric oxide, glucocorticoid therapy, IL-1 inhibition, motor symptoms, neurodegeneration
- MeSH terms
- Animals, Cells, Cultured, Dexamethasone, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Glucocorticoids, Interleukin-1, Lipopolysaccharides, Male, Nerve Degeneration, Nitric Oxide, Parkinson Disease, Psychomotor Performance, Substantia Nigra, Oxidopamine, Rats, Wistar, Microglia, Disease Progression, Reverse Transcriptase Polymerase Chain Reaction, Rats
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