Scientists have provided the first evidence of the close interactions between genes and the environment in the social dysfunctions typical of autistic disorders.
For the first time a team from the University of Geneva (UNIGE), Switzerland, within the framework of the Synapsy National Centre of Competence in Research, has deciphered how a change in cell environment triggers the onset of autistic symptoms in mice with a genetic vulnerability.
While a link between the inflammatory process and autism was suspected, an imbalance in the expression of a series of genes caused by a massive inflammation — resulting from an immune response to the administration of a pharmacological product —leads to the hyperexcitability of neurons of the reward system” says a press release from the University of Geneva (UNIGE), Switzerland.
“Humans carry a mutation in only one of the two copies of SHANK3, a gene that is essential for the functioning of synapses and communication between neurons,” points out Camilla Bellone. “In animal models of the disease, however, mutation of a single copy of SHANK3 only slightly affects the behaviour of mice, which explains why the behavioural phenotypes observed are not homogeneous”.