ArticleNeurotoxicity research2009
CXCR4 and CXCL12 expression is increased in the nigro-striatal system of Parkinson's disease.
Article in Neurotoxicity research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Neuroprotective Effects of Resveratrol in In vivo and In vitro Experimental Models of Parkinson's Disease: a Systematic Review.Neurotoxicity research · 2022Pooled it
- Adaptive immunity in the pathogenesis of neurodegeneration.Nature immunology · 2026Review
- Neurexins, Ephrin receptors, and N-cadherin signaling as emerging mechanisms in synaptic dysfunction and neurodegenerative diseases.Communications biology · 2026Review
- Immune and metabolic signatures characterise constipation-driven endophenotypes in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Soluble immune factor profiles in blood and CSF associated with LRRK2 mutations and Parkinson's disease.NPJ Parkinson's disease · 2025Article
- An update on the involvement of inflammatory mediators in Parkinson's disease pathogenesis.Archives of toxicology · 2025Review
- Mapping the peripheral immune landscape of Parkinson's disease patients with single-cell sequencing.Brain : a journal of neurology · 2025Article
- Unique nigral and cortical pathways implicated by epigenomic and transcriptional analyses in rotenone Parkinson's model.NPJ Parkinson's disease · 2025Article
- The role of CXCL12/CXCR4/CXCR7 axis in cognitive impairment associated with neurodegenerative diseases.Brain, behavior, & immunity - health · 2025Review
- Inflammatory Intracellular Signaling in Neurons Is Influenced by Glial Soluble Factors in iPSC-Based Cell Model ofInternational journal of molecular sciences · 2024Article
- SP1-Driven FOXM1 Upregulation Induces Dopaminergic Neuron Injury in Parkinson's Disease.Molecular neurobiology · 2024Article
- Cellular and molecular mechanisms of the blood-brain barrier dysfunction in neurodegenerative diseases.Fluids and barriers of the CNS · 2024Review
- Free water imaging in Parkinson's disease and atypical parkinsonian disorders.Journal of neurology · 2024Article
- CXCR4 as possible druggable target linking inflammatory bowel disease and Parkinson's disease.Metabolic brain disease · 2023Article
- HMGB1 is a Potential and Challenging Therapeutic Target for Parkinson's Disease.Cellular and molecular neurobiology · 2023Review
- Advances in NURR1-Regulated Neuroinflammation Associated with Parkinson's Disease.International journal of molecular sciences · 2022Review
- Multiomic Analyses of Dopaminergic Neurons Isolated from Human Substantia Nigra in Parkinson's Disease: A Descriptive and Exploratory Study.Cellular and molecular neurobiology · 2022Article
- Neuroinflammation and Parkinson's Disease-From Neurodegeneration to Therapeutic Opportunities.Cells · 2022Review
- Role of exosomes in the pathogenesis of inflammation in Parkinson's disease.Neural regeneration research · 2022Review
- Parkinson's disease peripheral immune biomarker profile: a multicentre, cross-sectional and longitudinal study.Journal of neuroinflammation · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Except for a handful of inherited cases related to known gene defects, Parkinson's disease (PD) is a sporadic neurodegenerative disease of unknown etiology. There is increasing evidence that inflammation and proliferation of microglia may contribute to the neuronal damage seen in the nigro-striatal dopaminergic system of PD patients. Microglia events that participate in neuronal injury include the release of pro-inflammatory and neurotoxic factors. Characterizing these factors may help to prevent the exacerbation of PD symptoms or to remediate the disease progression. In rodents, the nigro-striatal system exhibits high expression of the chemokine receptor CXCR4. Its natural ligand CXCL12 can promote neuronal apoptosis. Therefore, the present study investigated the expression of CXCR4 and CXCL12 in post-mortem brains of PD and control (non-PD) individuals and in an animal model of PD. In the human substantia nigra (SN), CXCR4 immunoreactivity was high in dopaminergic neurons. Interestingly, the SN of PD subjects exhibited higher expression of CXCR4 expression and CXCL12 than control subjects despite the loss of dopamine (DA) neurons. This effect was accompanied by an increase in activated microglia. However, results from post-mortem brains may not provide indication as to whether CXCL12/CXCR4 can cause the degeneration of DA neurons. To examine the role of these chemokines, we determined the levels of CXCL12 and CXCR4 in the SN of MPTP-treated mice. MPTP produced a time-dependent up-regulation of CXCR4 that preceded the loss of DA neurons. These results suggest that CXCL12/CXCR4 may participate in the etiology of PD and indicate a new possible target molecule for PD.
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