ArticleCells2023
Toll-like Receptor 4 Is Upregulated in Parkinson's Disease Patients and Co-Localizes with pSer129αSyn: A Possible Link with the Pathology.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Parabacteroides goldsteinii mitigates parkinsonism in LRRK2 mutant mice by reducing neuroinflammation through Gut-Brain axis.Journal of advanced research · 2026Article
- Genetically predicted CXCL16 expression is associated with Parkinson's disease risk and peripheral immune cell dysregulation: a two-sample mendelian randomization study.Molecular brain · 2026Article
- Molecular Mechanisms and Network Pharmacology Revealing Therapeutic Potential of Acetamidosulfonamides against Parkinsonian Model.ACS omega · 2026Article
- Systemic Endotoxemia, Inflammatory Activation, and Lipid Dysregulation in Parkinson's Disease: Evidence from Circulating LPS-Related Biomarkers and Plasma Lipids.International journal of molecular sciences · 2026Article
- Microglia, Astrocytes, and Oligodendrocytes in Parkinson's Disease: Neuroinflammatory Crosstalk and Emerging Therapeutic Strategies.Biomolecules · 2026Review
- Farnesol, a Dietary Sesquiterpene, Attenuates Rotenone-Induced Dopaminergic Neurodegeneration by Inhibiting Oxidative Stress, Inflammation, and Apoptosis via Mediation of Cell Signaling Pathways in Rats.International journal of molecular sciences · 2026Article
- Paeonol Mitigates Neurodegeneration: Molecular Insights into Its Anti-inflammatory, Antioxidant, and Synaptoprotective Mechanisms.Molecular neurobiology · 2025Review
- Role of Cellular Senescence in Parkinson's Disease: Potential for Disease-Modification Through Senotherapy.Biomedicines · 2025Review
- Pro-Oxidative and Inflammatory Actions of Extracellular Hemoglobin and Heme: Molecular Events and Implications for Alzheimer's and Parkinson Disease.Biomolecules & therapeutics · 2025Review
- The microbiota-gut-brain axis: a potential target in the small-molecule compounds and gene therapeutic strategies for Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- TNBS colitis induces architectural changes and alpha-synuclein overexpression in mouse distal colon: A morphological study.Cell and tissue research · 2025Article
- The immune system in Parkinson's disease: what we know so far.Brain : a journal of neurology · 2024Review
- Review
- From Immunity to Neurogenesis: Toll-like Receptors as Versatile Regulators in the Nervous System.International journal of molecular sciences · 2024Review
- The role of neuroinflammation in neurodegenerative diseases: current understanding and future therapeutic targets.Frontiers in aging neuroscience · 2024Review
- Plasma level of alpha-synuclein oligomers as a biomarker for isolated rapid eye movement sleep behavior disorder diagnosis and progression: a prospective cohort study.Frontiers in neurology · 2024Article
- Shedding light on the molecular and regulatory mechanisms of TLR4 signaling in endothelial cells under physiological and inflamed conditions.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growing evidence suggests a crucial role of neuroinflammation in the pathophysiology of Parkinson's disease (PD). Neuroinflammation is linked to the accumulation and aggregation of a-synuclein (αSyn), the primary pathological hallmark of PD. Toll-like receptors 4 (TLR4) can have implications in the development and progression of the pathology. In this study, we analyzed the expression of TLR4 in the substantia nigra (SN) and medial temporal gyrus (GTM) of well-characterized PD patients and age-matched controls. We also assessed the co-localization of TLR4 with pSer129 αSyn. Using qPCR, we observed an upregulation of TLR4 expression in the SN and GTM in PD patients compared to controls, which was accompanied by a reduction in αSyn expression likely due to the depletion of dopaminergic (DA) cells. Additionally, using immunofluorescence and confocal microscopy, we observed TLR4-positive staining and co-localization with pSer129-αSyn in Lewy bodies of DA neurons in the SN, as well as in pyramidal neurons in the GTM of PD donors. Furthermore, we observed a co-localization of TLR4 and Iba-1 in glial cells of both SN and GTM. Our findings provide evidence for the increased expression of TLR4 in the PD brain and suggest that the interaction between TLR4 and pSer129-αSyn could play a role in mediating the neuroinflammatory response in PD.
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