Impact of early-life microbiota depletion on central and enteric neurodysfunctions in a mouse model of demyelination

The aim of this research thesis was to characterize the role of the microbiota-gut-brain axis on the structural and functional integrity of the central and enteric nervous system in an experimental model of demyelination induced by the oral administration of the neurotoxin cuprizone. Then, by using experimental manipulation of the microbiota, we explored the role of host-microbiota interactions in MS-associated GI disease and their relationship to cognition. Molecular, biochemical, and functional assays were performed to identify the critical pathophysiological pathways that affect gut homeostasis probably preceding the onset of central signs/symptoms, as well as to evaluate the effect of gut microbiome dysbiosis on the severity of demyelination.