ArticleNeurotoxicity research2017
A20 in Multiple Sclerosis and Parkinson's Disease: Clue to a Common Dysregulation of Anti-Inflammatory Pathways?
Article in Neurotoxicity research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- The Footprints of Poly-Autoimmunity: Evidence for Common Biological Factors Involved in Multiple Sclerosis and Hashimoto's Thyroiditis.Frontiers in immunology · 2018Trial
- Regulator of G protein signaling 10: a critical regulator of chronic systemic inflammation in parkinson's disease.Journal of neuroinflammation · 2026Review
- Integrated bioinformatics identifies ferroptosis biomarkers and therapeutic targets in idiopathic pulmonary arterial hypertension.Scientific reports · 2025Article
- Inflammatory Intracellular Signaling in Neurons Is Influenced by Glial Soluble Factors in iPSC-Based Cell Model ofInternational journal of molecular sciences · 2024Article
- Involvement of KAntioxidants (Basel, Switzerland) · 2024Article
- A Model of iPSC-Derived Macrophages withInternational journal of molecular sciences · 2023Article
- Experimental Analysis of Tear Fluid and Its Processing for the Diagnosis of Multiple Sclerosis.Sensors (Basel, Switzerland) · 2023Article
- Identification of ferroptosis related biomarkers and immune infiltration in Parkinson's disease by integrated bioinformatic analysis.BMC medical genomics · 2023Article
- Necroptosis and Alzheimer's Disease: Pathogenic Mechanisms and Therapeutic Opportunities.Journal of Alzheimer's disease : JAD · 2023Review
- The impact of pre-freezing storage time and temperature on gene expression of blood collected in EDTA tubes.Molecular biology reports · 2022Article
- Article
- Exploring the key ferroptosis-related gene in the peripheral blood of patients with Alzheimer's disease and its clinical significance.Frontiers in aging neuroscience · 2022Article
- Deubiquitinating enzymes (DUBs): decipher underlying basis of neurodegenerative diseases.Molecular psychiatry · 2022Review
- Experimental colitis promotes sustained, sex-dependent, T-cell-associated neuroinflammation and parkinsonian neuropathology.Acta neuropathologica communications · 2021Article
- Overexpression of the ubiquitin-editing enzyme A20 in the brain lesions of Multiple Sclerosis patients: moving from systemic to central nervous system inflammation.Brain pathology (Zurich, Switzerland) · 2021Article
- Tumour Necrosis Factor Alpha-induced Protein 3 Negatively Regulates Cutibacterium acnes-induced Innate Immune Events in Epidermal Keratinocytes.Acta dermato-venereologica · 2021Article
- Deubiquitinase OTUD6A promotes proliferation of cancer cells via regulating Drp1 stability and mitochondrial fission.Molecular oncology · 2020Article
- TNFAIP3 Deficiency Affects Monocytes, Monocytes-Derived Cells and Microglia in Mice.International journal of molecular sciences · 2020Article
- Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation significantly contributes to the pathogenesis of several neurodegenerative disorders. In physiological conditions, a chronic inflammatory state is prevented through the termination of the acute inflammatory response once the triggering insult is eliminated. Several mechanisms regulate the resolution of inflammation. Among these, a potent inhibitor of the pro-inflammatory NF-kB signaling known as A20 has emerged as a key player. Recent studies have shown reduced blood levels of A20 in the patients of diverse chronic inflammatory diseases. Similar results have also been demonstrated in patients of multiple sclerosis (MS), a neurodegenerative disease characterized by persisting inflammation. In the present study, we investigate whether other similar neurodegenerative disorders such as Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS) also demonstrate deregulated levels of A20 expression as compared to healthy controls (HC) and treatment-naive MS patients. Our results confirm previous data that the A20 expression is reduced in whole blood of MS patients as compared to HC. Additionally, we demonstrate that significantly diminished A20 expression is also evident in PD patients. The dysregulation of the A20 pathway could then contribute to the persistence of inflammation in these disorders. It would thus be interesting to investigate further whether such commonly deregulated pathways between different inflammatory diseases could represent novel targets for therapy.
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