• Sylvie Tordjman, Eszter Somogyi, Nathalie Coulon, Solenn Kermarrec, David Cohen, Guillaume Bronsard, Olivier Bonnot, Catherine Weismann-Arcache, Michel Botbol, Bertrand Lauth, Vincent Ginchat, Pierre Roubertoux, Marianne Barburoth, Viviane Kovess, Marie-Maude Geoffray, and Jean Xavier.
• Laboratoire Psychologie de la Perception, Université Paris Descartes, CNRS UMR 8158 , Paris , France ; Pôle Hospitalo-Universitaire de Psychiatrie de l'Enfant et de l'Adolescent, Université de Rennes 1, Centre Hospitalier Guillaume Régnier , Rennes , France.
• Front Psychiatry. 2014 Jan 1; 5: 53.

AbstractSeveral studies support currently the hypothesis that autism etiology is based on a polygenic and epistatic model. However, despite advances in epidemiological, molecular and clinical genetics, the genetic risk factors remain difficult to identify, with the exception of a few chromosomal disorders and several single gene disorders associated with an increased risk for autism. Furthermore, several studies suggest a role of environmental factors in autism spectrum disorders (ASD). First, arguments for a genetic contribution to autism, based on updated family and twin studies, are examined. Second, a review of possible prenatal, perinatal, and postnatal environmental risk factors for ASD are presented. Then, the hypotheses are discussed concerning the underlying mechanisms related to a role of environmental factors in the development of ASD in association with genetic factors. In particular, epigenetics as a candidate biological mechanism for gene × environment interactions is considered and the possible role of epigenetic mechanisms reported in genetic disorders associated with ASD is discussed. Furthermore, the example of in utero exposure to valproate provides a good illustration of epigenetic mechanisms involved in ASD and innovative therapeutic strategies. Epigenetic remodeling by environmental factors opens new perspectives for a better understanding, prevention, and early therapeutic intervention of ASD.

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