Contributions
Abstract: EP1415
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - Inflammation and tissue damage
The acute inflammatory response is normally terminated once the triggering insult is eliminated. If it does not occur properly, a chronic inflammatory state may be ensued. Growing evidences refer to the chronic inflammation as a contributor to the pathogenesis of several neurodegenerative disorders. For this reason, several key regulatory mechanisms are normally involved in the resolution of inflammation. Among these, A20, the most potent inhibitor of the pro-inflammatory NF-kB signaling, plays a key role in the regulation of inflammation. Recently, reduced levels of A20 were described in peripheral blood cells of patients affected by Multiple Sclerosis (MS), a chronic neurological inflammatory disease.
Here we investigated whether chronic neurodegenerative disorders characterized by inflammation show deregulated A20 levels. We measured A20 gene expression by real-time PCR in whole blood of 20 patients affected by Parkinson"s disease (PD), 20 by Alzheimer"s disease (AD), 36 by Amyotrophic Lateral Sclerosis (ALS) and in 40 healthy controls and 34 treatment-naive MS patients.
We confirmed that A20 levels are reduced in whole blood from MS patients compared to HC. Moreover, we observed that also A20 expression in PD patients is lower compared to HC. These results suggest that MS and PD could share a common regulatory mechanism of inflammation resolution, consisting in the anti-inflammatory signaling involving A20. The deregulation of this braking pathway, due to the A20 down-regulation, could contribute to the pathogenesis of these disorders, leading in turn to the exacerbation of neurodegenerative processes.
Disclosure: The study was supported by grants from the Fondazione Italiana Sclerosi Multipla (FISM - Grant number 2010/R/7), from the Italian Ministry of Health (Bando Giovani Ricercatori 2010- Grant agreement GR-2010-2315964) and the European Community´s Health Seventh Framework Programme (FP7/2007-2013 under grant agreement 259867). Perga, Martire, Montarolo, Navone, Calvo, Fuda, Marchet, Leotta, Chiò and Bertolotto: nothing to disclose.
Abstract: EP1415
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - Inflammation and tissue damage
The acute inflammatory response is normally terminated once the triggering insult is eliminated. If it does not occur properly, a chronic inflammatory state may be ensued. Growing evidences refer to the chronic inflammation as a contributor to the pathogenesis of several neurodegenerative disorders. For this reason, several key regulatory mechanisms are normally involved in the resolution of inflammation. Among these, A20, the most potent inhibitor of the pro-inflammatory NF-kB signaling, plays a key role in the regulation of inflammation. Recently, reduced levels of A20 were described in peripheral blood cells of patients affected by Multiple Sclerosis (MS), a chronic neurological inflammatory disease.
Here we investigated whether chronic neurodegenerative disorders characterized by inflammation show deregulated A20 levels. We measured A20 gene expression by real-time PCR in whole blood of 20 patients affected by Parkinson"s disease (PD), 20 by Alzheimer"s disease (AD), 36 by Amyotrophic Lateral Sclerosis (ALS) and in 40 healthy controls and 34 treatment-naive MS patients.
We confirmed that A20 levels are reduced in whole blood from MS patients compared to HC. Moreover, we observed that also A20 expression in PD patients is lower compared to HC. These results suggest that MS and PD could share a common regulatory mechanism of inflammation resolution, consisting in the anti-inflammatory signaling involving A20. The deregulation of this braking pathway, due to the A20 down-regulation, could contribute to the pathogenesis of these disorders, leading in turn to the exacerbation of neurodegenerative processes.
Disclosure: The study was supported by grants from the Fondazione Italiana Sclerosi Multipla (FISM - Grant number 2010/R/7), from the Italian Ministry of Health (Bando Giovani Ricercatori 2010- Grant agreement GR-2010-2315964) and the European Community´s Health Seventh Framework Programme (FP7/2007-2013 under grant agreement 259867). Perga, Martire, Montarolo, Navone, Calvo, Fuda, Marchet, Leotta, Chiò and Bertolotto: nothing to disclose.