Hypothesis and Preliminary Results on the Role of MUC1 and MUC2 in Relationship to Autism AetiologyAuthor(s): Menicagli Roberto* and Limodio Marta
Background: Aim autism a neurological disorder with either genetic or environmental component Autism generally presents changes of intestinal permeability to produce metabolism’s alteration in the gastrointestinal tract The intestinal macrobiota produces metabolites, opioid like peptides, that show properties experimentally associated with autism The aim of this study it is to understand the cause of intestinal permeability’s alteration
Materials and methods: We determinate the intestinal MUC2, on stool samples of twelve Patient, and healthy control, with Fecal Mucin Assay and analyzed the results with Mann-Whitney U Test Calculator
Results: The results of the dosage of MUC2’concentration in autistic people decrease vs and healthy control groups: this result is statistically significant: the p-value is 00124
Discussion: The result shows a increase of MUC2, perhaps of genetic origin We hypnotize also a probable over expression on highly ipoglicosilated MUC1. All this prevents a regular linkage of the MUC2 to the MUC1, so to form many channels in mucosa The free MUC2 relying on themselves and join together with hydrogen bridge bonds, leaving the highly glycosylated end parts to become the starting point for abnormal growth of the bacteria, which in turn produce opioid such as peptides, that pass into the channels of the mucosa layer.