CX3CL1 reduces neurotoxicity and microglial activation in a rat model of Parkinson’s disease
Open accessAbstract
BACKGROUND: Parkinson's disease is characterized by a progressive loss of dopaminergic neurons in the substantia nigra. The cause of the neurodegeneration is unknown. Neuroinflammation has been clearly shown in Parkinson's disease and may be involved in the progressive nature of the disease. Microglia are capable of producing neuronal damage through the production of bioactive molecules such as cytokines, as well as reactive oxygen species (ROS), and nitric oxide (NO). The inflammatory response in the brain is tightly regulated at multiple levels. One form of immune regulation occurs via neurons. Fractalkine (CX3CL1), produced by neurons, suppresses the activation of microglia. CX3CL1 is constitutively expressed. It is not known if addition of exogenous CX3CL1 beyond otherwise physiologically normal levels could decrease microglia activation and thereby minimize the secondary neurodegeneration following a neurotoxic insult. METHODS: The intrastriatal 6-hydroxydopamine (6-OHDA) rat model of Parkinson disease, was used to test the hypothesis that exogenous CX3CL1 could be neuroprotective. Treatment with recombinant CX3CL1 was delivered to the striatum by an osmotic minipump for 28 days beginning 7 days after the initial insult. Unbiased stereological methods were used to quantify the lesion size in the striatum, the amount of neuronal loss in the substantia nigra, and the amount of microglia activation. RESULTS: As hypothesized, CX3CL1 was able to suppress this microglia activation. The reduced microglia activation was found to be neuroprotective as the CX3CL1 treated rats had a smaller lesion volume in the striatum and importantly significantly fewer neurons were lost in the CX3CL1 treated rats. CONCLUSION: These findings demonstrated that CX3CL1 plays a neuroprotective role in 6-OHDA-induced dopaminergic lesion and it might be an effective therapeutic target for many neurodegenerative diseases, including Parkinson disease and Alzheimer disease, where inflammation plays an important role.
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The reduction in microglia activation in the α-Syn Parkinson's disease model may be caused in part by Spirulina enhancing microglial expression of the fractalkine receptor CX3CR1, which is neuroprotective in a 6-OHDA Parkinson's disease model.
“The reduction in microglia activation may be caused, in part, by Spirulina’s capacity to enhance expression on the microglia of the fractalkin receptor (CX3CR1), which is neuroprotective in a 6-OHDA model of PD [126].”
From Beneficial Effects of Spirulina Consumption on Brain Health (2022) · cites this paper as [126]
Spirulina was neuroprotective in an α-Syn rat model of Parkinson's disease, increasing TH+ and NeuN+ cells and decreasing activated microglial cells as evaluated by MHC II expression.
“The authors showed that Spirulina was neuroprotective in this α-Syn model of PD, observing a major number of TH+ and NeuN+ cells and a decrease in the number of activated microglial cells as evaluated by MHC II expression.”
From Beneficial Effects of Spirulina Consumption on Brain Health (2022) · cites this paper as [126]
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- Authors
- Pabon, M. M., Bachstetter, A. D., Hudson, C. E., Gemma, C., & Bickford, P. C.
- Affiliations
- University of South Florida (US)
- University of Kentucky (US)
- James A. Haley Veterans' Hospital (US)
- Corresponding author
- Gemma, Carmelina
- Bickford, Paula C
- Venue
- Journal of Neuroinflammation
- Published
- 2011-01-25
- Volume
- 8
- Issue
- 1
- Pages
- 9-9
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3039584
- OpenAlex
- W2163743819
- Cited by
- 241
- References
- 21
- Citations by year
- 2026: 9 · 2025: 13 · 2024: 24 · 2023: 13 · 2022: 17 · 2021: 14 · 2020: 13 · 2019: 21 · 2018: 14 · 2017: 11 · 2016: 20 · 2015: 16 · 2014: 20 · 2013: 17 · 2012: 13
- FWCI
- 9.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UKnowledge (University of Kentucky) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R21AG024165, P01 AG04418, F32AG037280, P01AG004418)
- 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
- fractalkine, Parkinson's disease, microglial activation, neuroinflammation, neuroprotection, 6-hydroxydopamine, dopaminergic neuron loss, substantia nigra, striatum, neurodegeneration, recombinant protein therapy
- MeSH terms
- Animals, Corpus Striatum, Disease Models, Animal, Humans, Male, Nerve Degeneration, Neurons, Parkinson Disease, Rats, Inbred F344, Substantia Nigra, Oxidopamine, Microglia, Rats, Chemokine CX3CL1
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