Abstract
Nurr1 plays anti-inflammatory functions in astrocytes/microglia. Gene expression analysis reveals Nurr1 down-regulation in PBMCs of MS patients that negatively correlates with disease aggressiveness. This study assesses the consequences of Nurr1 reduction in a MS model represented by EAE. EAE was induced in heterozygous Nurr1 knockout mice. Clinical course was evaluated during pre-symptomatic, acute, and chronic phases. Neurohistopathological state was analyzed in spinal cord. Nurr1 defect induces early EAE onset and increases inflammatory infiltrates in spinal cord suggesting a Nurr1 role in the early phase of EAE.
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