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A large study by researchers with the UC Davis MIND Institute has found that a gene whose role is to suppress cellular damage from environmental stressors is nearly twice as likely to be defective in children with autism spectrum disorder (ASD), and that the deficit is also present in their fathers.
The correlation is particularly high among children with more severe ASD, a developmental disorder whose hallmarks are communication and learning delays and often intellectual disability. The study is published online in Pediatrics, the journal of the American Academy of Pediatrics.
“In the presence of some type of environmental stressor, the tumor suppressor p53 stops cell division to allow the repair of damaged DNA ,” said senior study author Cecilia Giulivi, professor and director of the Redox Biology Lab at UC Davis, and an affiliate of the MIND Institute.
The research was conducted in 2- to 5-year-olds using blood samples from 66 children with autism and their parents and 46 same-aged typically developing children and their parents, all of whom participate in the Childhood Autism Risks from Genetics and Environment (CHARGE) Study at UC Davis.
Read full, original post: ‘Cancer gene’ twice as likely to be defective in children with autism
