Identification of molecular targets for mycotoxins related to autism development

Motivations Autistic spectrum disorder (ASD) is an ensemble of developmental disorders impacting on the social relationships, the development of the language and of interpersonal communications and the behaviour of affected people. A number of factors have been supposed to cause ASD, including a direct genetic component (accounting for less than 10% of cases), epigenetics and environmental factors such as pollutants, heavy metals, viruses and vaccines. To date, however, none of these factors have been definitely associated to ASD. Further studies hypothesized the presence of “vulnerability genes” whose variants are not causative of autism per se, but can increase the susceptivity of the individuals towards several factors, ultimately leading to autism development. In people with ASD, gastrointestinal (GI) disorders are commonly reported. The “leaky gut hypothesis” theory speculates that impaired gut permeability permits the entry of molecules such as toxins in the bloodstream, both affecting directly the central nervous system (CNS), and causing sensitization of the gut mucosal immune system. Mycotoxins are food contaminants present ubiquitously and derived from the secondary metabolism of several moulds and fungi. The consumption of several foods, especially those derived from cereals and milk, exposes people to the intake of high level of mycotoxins. Children can be more exposed than adults to mycotoxins, for their particular diet, for a lower diet variability with respect to adults, and for the fact that a newborn assumes more food than an adult, in proportion to his/her body weight. Once introduced in the body, mycotoxins could promote sneaky negative effects in the GI trait and in other tissues, playing a role in the development of syndromes of unknown etiology. In our work, we used bioinformatics approaches to find potential targets for the binding of mycotoxins, in order to verify the existence of a possible role in ASD onset, and we tested a small sample of ASD patients and controls to verify the alteration of genes identified as potential targets.