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Synuclein activates microglia in a model of Parkinson's disease
Open accessAbstract
Parkinson's disease (PD) is the most common neurodegenerative movement disorder afflicting >500,000 patients in the United States alone. This age-related progressive disorder is typified by invariant loss of dopaminergic substantia nigra neurons (DAN), dystrophic neurites, the presence of alpha-synuclein (SYN) positive intracytoplasmic inclusions (Lewy bodies) in the remaining DAN, and activated microglia. As such, microglial activation and resultant increase in proinflammatory molecules have moved to the forefront of PD research as a potential pathobiologic mechanism of disease. Herein, we present data demonstrating early microglial activation in mice that over-express wild-type SYN, the release of SYN from a SYN overexpressing MN9D cell line, and dose-dependent SYN-mediated activation of primary microglial cultures with consequent increases in proinflammatory molecules. Furthermore, we provide evidence that the CD36 scavenger receptor and downstream kinases are involved in SYN-mediated microglial activation. Together, our data suggest an early role for SYN and inflammation in PD pathogenesis.
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“SR-B2 promotes α-synuclein–microglial interactions64 and senses misfolded mutant or oxidized SOD1 in diseased motor neurons or in the extracellular space, rendering these cells proinflammatory85.”
From Microglia in neurodegeneration (2018) · cites this paper as [64]
In the citing paper
“Microglia accumulate near α-synuclein deposits and become proinflammatory in a manner dependent on receptors that also bind Aβ, such as CD36 and TLR263–65.”
From Microglia in neurodegeneration (2018) · cites this paper as [64]
In the citing paper
“Microglia also phagocytose α-synuclein, the constituent protein of Lewy bodies in Parkinson’s and Lewy Body dementias, and become pro-inflammatory in the process, expressing cytokines (IL1β, IL6, TNFα), reactive oxygen species (ROS) and prostaglandin synthesising cyclooxygenase 2 (COX2) [24,25,26].”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [25]
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“…as a pathogen-or damage-associated molecular pattern (DAMP or PAMP, respectively), as demonstrated by the fact that α -Syn can engage TLR2 [100,101] and TLR4 [102], as well as the evidence that the ablation of CD36 from mice-derived glia leads to a less severe activation in these cells [103].”
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“These studies rapidly converted the α-syn TG-mice and rats into the main animal models used for studying PD.”
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“However, as the function of SYN is not completely understood and, in culture models of SYN overexpression this protein is released, the existence of extracellular SYN and its role should not be discounted (Lee et al. 2005; Su et al. 2008).”
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“A number of studies have shown that following SCI, proinflammatory cytokines like Interleukin-1 (IL-1) and Tumor Necrosis Factor-α (TNF-α) are elevated in the injured spinal cord [3].”
BackgroundInfluentialImmunological aspects of Parkinson's disease
Belova, O. V., Arefieva, T. I., & Moskvina, S. N. (2020) · S S Korsakov Journal of Neurology and Psychiatry · doi:10.17116/jnevro2020120021110 · Cited by 8
Park, S., Nozaki, K., Smith, J. A., Krause, J. S., & Banik, N. L. (2013) · Journal of Neurochemistry · doi:10.1111/jnc.12520 · Cited by 7
“…that cytokine involvement in various neurodegenerative disease including AD (Rogers and Lue 2001; Swardfager et al. 2010), Parkinson’s disease (Sawada et al. 2006; Gao et al. 2008; Su et al. 2008), ALS (Sekizawa et al. 1998; Ono et al. 2001), and SCI (Guerrero et al. 2012; Thompson et al. 2013).”
BackgroundCampomayor, N. B., Kim, H. J., & Kim, M. (2025) · Biomolecules & Therapeutics · doi:10.4062/biomolther.2024.224 · Cited by 8
“Ablation of microglial CD36 has been shown to result in decreased phagocytosis of monomeric α -syn and reduced TNF-α expression (Su et al ., 2008; Ferreira and Romero-Ramos, 2018).”
Carneiro-Pereira, B., Ferreira-Antunes, F., Campos, J., Salgado, A. J., & Sampaio‐Marques, B. (2025) · Molecules · doi:10.3390/molecules30112260 · Cited by 6
“Interestingly, several lines of evidence suggest that activated microglial cells directly engulf asyn in an attempt to clear it from the extracellular space, either as a result of apoptotic neuron death or from mecha-Molecules nisms of cellular release [72–75].”
De, S., Banerjee, S., Rakshit, P., Banerjee, S., & Kumar, S. K. A. (2024) · Current Diabetes Reviews · doi:10.2174/0115733998291968240429111357 · Cited by 6
Does a prion-like mechanism play a major role in the apparent spread of α-synuclein pathology?
Sacino, A. N., & Giasson, B. I. (2012) · Alzheimer s Research & Therapy · doi:10.1186/alzrt151 · Cited by 6
“Although α-synuclein was viewed typically as a cytoplasmic protein, investigators have shown that both soluble and aggregated α-synuclein can be released from cells [25,26] and that α-synuclein is present in brain inter stitial fl uid, cerebrospinal fl uid, and blood plasma [26-30].”
Oxidative Stress in Parkinson’s Disease: Role in Neurodegeneration and Targets for Therapeutics
Banerjee, R., Kaidery, N. A., & Thomas, B. (2015) · ACS symposium series · doi:10.1021/bk-2015-1200.ch005 · Cited by 7
An Update on CSF Biomarkers of Parkinson’s Disease
LeWitt, P. A., Huber, B. R., & Zhang, J. (2012) · Advances in predictive, preventive and personalised medicine · doi:10.1007/978-94-007-5866-7_8 · Cited by 6
Wang, Y., Gao, P.-P., Wu, Z., Jiang, B., Wang, Y., He, Z., Zhao, B., Tian, X., Gao, H., Cai, L., et al. (2024) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2024.119095 · Cited by 6
Autophagy and Parkinsons Disease-Role of Caffeine as Autophagic Stimulator and Anti Apoptotic Agent
Surendran, S., Suresh, G., Vijayakumar, N., & Ramachandran, R. (2023) · Nepal Journal of Biotechnology · doi:10.54796/njb.v11i2.262 · Cited by 5
Nanocarriers to mediate the pathways from diabetes toward Parkinson's disease
De, S., & Kuo, Y. (2024) · Journal of the Taiwan Institute of Chemical Engineers · doi:10.1016/j.jtice.2024.105401 · Cited by 6
Immunotherapeutic interventions in Parkinson's disease: Focus on α-Synuclein
Ganguly, U., Singh, S., Chakrabarti, S., Saini, A. K., & Saini, R. V. (2022) · Advances in protein chemistry and structural biology · doi:10.1016/bs.apcsb.2021.11.010 · Cited by 6
Vaquero-Rodríguez, A., Razquin, J., Murueta‐Goyena, A., Miguélez, C., Ruíz-Ortega, J. Á., Lafuente, J. V., Bengoetxea, H., & Ortuzar, N. (2025) · Brain Structure and Function · doi:10.1007/s00429-025-02959-9 · Cited by 6
“…the permitted use, you will need to obtain permission directly from the copyright have been described in other animal models of PD, where an increase in the glial population has been described in both neurotoxic (Farrand et al. 2017) and transgenic models (Su et al. 2008; Watson et al. 2012).”
Klæstrup, I. H., Reinert, L. S., Ferreira, S. A., Lauritsen, J., Toft, G. U., Gram, H., Jensen, P. H., Paludan, S. R., & Romero‐Ramos, M. (2025) · npj Parkinson s Disease · doi:10.1038/s41531-025-01228-0 · Cited by 5
“Aggregated α -syn can be recognized and bind to receptors on microglia, such as the toll-like receptors (TLR) 2 and TLR4 9 – 13 , thereby activating downstream pathways such as the NF-κ B signaling and NLRP3 in fl ammasome assembly 9 .”
Menopause triggers microglia-associated neuroinflammation in Parkinson’s disease
Usman, S., & Mondal, A. C. (2025) · Brain Research · doi:10.1016/j.brainres.2025.149649 · Cited by 5
Huang, L., Shimoji, M., Wang, J., Shah, S., Kamila, S., Biehl, E. R., Lim, S., Chang, A., Maguire‐Zeiss, K. A., Su, X., et al. (2013) · Neurotherapeutics · doi:10.1007/s13311-013-0208-3 · Cited by 6
“Full-length complementary DNA of LRRK2WT or LRRK2G2019S was amplified by high-fidelity PCR and cloned into the pBig2iFLAGSocs6IRES2eGFP, which is a tetracyclineresponsive autoregulated bi-directional expression vector with an IRESeGFP cassette [39, 40].”
MethodSelf-citationPerspective on Cav-1 for its Potential as Newer Therapeutics for Parkinson’s Disease
Singh, G., Pushpa, T., Gupta, S., Srivastava, S., Khatri, D. K., & Singh, S. B. (2022) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527321666220909150406 · Cited by 3
Varma, M., Bhandari, R., & Kuhad, A. (2023) · Metabolic Brain Disease · doi:10.1007/s11011-023-01247-x · Cited by 4
“…which is an important marker present in the brains of PD patients, is believed to activate the ERK pathway among others in microglial cells (Su et al. 2008), and this causes the release of tumor-necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β), bringing about an inflam - mation…”
BackgroundMitochondria at the Base of Neuronal Innate Immunity in Alzheimer’s and Parkinson’s Diseases
Esteves, A. R., Silva, D. F., Santos, D., Candeias, E., Filipe, F., & Cardoso, S. M. (2018) · InTech eBooks · doi:10.5772/intechopen.72612 · Cited by 4
“[212] Su X, Maguire-Zeiss KA, Giuliano R, Prifti L, Venkatesh K, Federoff HJ.”
BackgroundThe Mediating Role of Inflammation in the Relationship Between α-Synuclein and Cognitive Functioning
Dabiri, S., Ramirez-Ruiz, M., Jean‐Louis, G., Ntekim, O. E., Obisesan, T. O., Campbell, A. L., Mwendwa, D. T., & Initiative, A. D. N. (2022) · The Journals of Gerontology Series A · doi:10.1093/gerona/glac217 · Cited by 3
Inflammasome-Mediated Inflammation in Neurodegenerative Diseases
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Klein, S. (2020) · USURJ University of Saskatchewan Undergraduate Research Journal · doi:10.32396/usurj.v6i2.425 · Cited by 3
Li, C., Hou, B., Li, X., Yang, Z., & Xie, A. (2022) · Neuroscience Letters · doi:10.1016/j.neulet.2022.136736 · Cited by 3
Effect of chlorpyrifos on cypermethrin-induced dopaminergic neurotoxicity in rats
Rawat, N., & Singh, M. P. (2024) · Toxicology and Industrial Health · doi:10.1177/07482337241267192 · Cited by 3
“Over-expression of α -synuclein- induced microglial activation led to the elevation of TNF-α , IL-1 β and COX-2 (Su et al., 2008).”
Revisiting the advance of age-dependent α-synuclein propagation and aggregation
Song, D., & Li, J. (2025) · Ageing and Neurodegenerative Diseases · doi:10.20517/and.2024.44 · Cited by 4
Razia, R., Majeed, F., Amin, R., Mukhtar, S. M., Mahmood, K., Abualait, T., Bashir, S., & Baig, D. N. (2023) · PLoS ONE · doi:10.1371/journal.pone.0285022 · Cited by 5
Microglial activation in a mouse model of α-synuclein overexpression
Maguire‐Zeiss, K. A., Su, X., & Federoff, H. J. (2008) · Elsevier eBooks · doi:10.1016/b978-0-12-374028-1.00040-3 · Cited by 3
Self-citation[Use of sodium diclofenac in acute renal colic].
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Jellinger, K. A., & Krismer, F. (2013) · Springer eBooks · doi:10.1007/978-3-7091-0687-7_4 · Cited by 3
Metadata
- Authors
- Su, X., Maguire-Zeiss, K. A., Giuliano, R., Prifti, L., Venkatesh, K., & Federoff, H. J.
- Affiliations
- University of Rochester Medicine (US)
- Corresponding author
- Federoff, Howard J.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2008-11
- Volume
- 29
- Issue
- 11
- Pages
- 1690-1701
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC2621109
- OpenAlex
- W2120997873
- Cited by
- 474
- References
- 86
- Citations by year
- 2026: 11 · 2025: 17 · 2024: 27 · 2023: 19 · 2022: 46 · 2021: 46 · 2020: 37 · 2019: 30 · 2018: 26 · 2017: 18 · 2016: 15 · 2015: 22 · 2014: 32 · 2013: 21 · 2012: 24
- FWCI
- 12.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (T32NS007489)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, alpha-synuclein, microglial activation, neuroinflammation, CD36 scavenger receptor, proinflammatory molecules, Lewy bodies, MN9D cells, pathogenesis
- MeSH terms
- Animals, Cell Line, Disease Models, Animal, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Cytokines, Microglia, Parkinsonian Disorders, Mice, Synucleins
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