| ORIGINAL ARTICLE |
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| Year : 2022 | Volume
: 17
| Issue : 1 | Page : 61-64 |
Hypothesis and preliminary results on the role of MUC1 and MUC2 in relationship to autism etiology
Menicagli Roberto1, Limodio Marta2
1 Biochemical Department, Milan University, Milan, Italy
2 Pharmaceutical Researcher, Frosinone, Italy
Correspondence Address:
Dr. Menicagli Roberto
Martiri della Libertà 6°a, 20060 Mediglia
Italy
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jpn.JPN_224_20
Background: Autism is a neurological disorder with either genetic or environmental component. Autism generally presents changes of intestinal permeability to produce alteration of metabolism in the gastrointestinal tract. The intestinal macrobiota produces metabolites, opioid-like peptides, that show properties experimentally associated with autism. The aim of this study is to understand the cause of intestinal permeability’s alteration. Materials and Methods: We determined intestinal MUC2 on stool samples of 12 patients and healthy controls with Fecal Mucin Assay and analyzed the results with Mann–Whitney U-test calculator. Results: The results of the dosage of MUC2’s concentration in autistic people decrease when compared with those of healthy control groups: this result is statistically significant: the p-value is 0.00124. Discussion: The results show an increase of MUC2, perhaps due to genetic origin. We hypnotize a probable over expression on highly hypoglycosylated MUC1. All this prevents a regular linkage of MUC2 to MUC1, so as to form many channels in mucosa. The free MUC2 relies on themselves and joins 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.
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