DOI: 10.1007/s12640-017-9724-y Pages: 1-7
Article Type: SHORT COMMUNICATION

A20 in Multiple Sclerosis and Parkinson’s Disease: Clue to a Common Dysregulation of Anti-Inflammatory Pathways?

1. San Luigi Gonzaga University Hospital & Neuroscience Institute Cavalieri Ottolenghi (NICO), Neurobiology Unit, Neurologia 2 – CReSM (Regional Referring Center Multiple Sclerosis)

2. Neuroscience Institute Cavalieri Ottolenghi (NICO) University of Turin & AOU San Luigi, Neurobiology Unit, Neurologia 2 – CRESM (Regional Referring Center of Multiple Sclerosis)

3. University of Turin & Città della Scienza e della Salute University Hospital, “Rita Levi Montalcini” Department of Neuroscience, ALS (Amyotrophic Lateral Sclerosis) Expert Center (CRESLA)

4. Martini Hospital, Division of Neurology

Correspondence to:
Simona Perga
Tel: 0039 011 670 66 00
Email: simonaperga77@gmail.com

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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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  • Accepted: Mar 8, 2017
  • Online: Mar 23, 2017
  • Revised: Mar 2, 2017

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