Ochratoxin A as possible factor trigging autism and its male prevalence via epigenetic mechanism. (Articolo in rivista)

Type
Label
  • Ochratoxin A as possible factor trigging autism and its male prevalence via epigenetic mechanism. (Articolo in rivista) (literal)
Anno
  • 2015-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1179/1476830515Z.000000000186 (literal)
Alternative label
  • Mezzelani A, Raggi ME, Marabotti A, Milanesi L. (2015)
    Ochratoxin A as possible factor trigging autism and its male prevalence via epigenetic mechanism.
    in Nutritional neuroscience (Online); Maney Publishing, Leeds (Regno Unito)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Mezzelani A, Raggi ME, Marabotti A, Milanesi L. (literal)
Pagina inizio
  • 1 (literal)
Pagina fine
  • 4 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 2015 Jan 17. (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
  • 4 (literal)
Note
  • ubMe (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1: Institute of Biomedical Technologies, National Research Council, Via Fratelli Cervi 93, 20090 Segrate, MI, Italy 2: Scientific Institute, IRCCS Eugenio Medea, Bosisio Parini, Lecco, Italy 3: Department of Chemistry and Biology, University of Salerno, Via Giovanni Paolo II 132, 84084 Fisciano, SA, Italy (literal)
Titolo
  • Ochratoxin A as possible factor trigging autism and its male prevalence via epigenetic mechanism. (literal)
Abstract
  • The role of dysbiosis causing leaky gut with xenobiotic production and absorption is increasingly demonstrated in autism spectrum disorder (ASD) pathogenesis. Among xenobiotics, we focused on ochratoxin A (one of the major food contaminating mycotoxin), that in vitro and in vivo exerts a male-specific neurotoxicity probably via microRNA modulation of a specific target gene. Among possible targets, we focused on neuroligin4X. Interestingly, this gene carries some SNPs already correlated with the disease and with illegitimate microRNA binding sites and, being located on X-chromosome, could explain the male prevalence. In conclusion, we propose a possible gene-environment interaction triggering ASD explaining the epigenetic neurotoxic mechanism activated by ochratoxin A in genetically predisposed children. This mechanism offers a clue for male prevalence of the disease and may have an important impact on prevention and cure of ASD. (literal)
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