Mice lacking the autism-associated SHANK3 gene were more sensitive to sensation, including touch. The mice also had overactive excitatory neurons in the somatosensory cortex, which may account for sensory hypersensitivity.
Mothers who were prescribed macrolide antibiotics, including erythromycin and azithromycin, early in pregnancy had an increased risk of their child being born with malformations, specifically cardiovascular malformations. However, researchers found no link between exposure to these antibiotics and an increased risk of neurodevelopmental disorders.
Higher gestational concentrations of phthalate metabolites were associated with an increased risk of autism in boys, but not in girls. Folic acid may help to protect against the effects of phthalate exposure, researchers report.
Study will analyze dried blood spots from newborns for over 1,000 different chemicals and molecules. The presence of some of the molecules may predict autism risk years before symptoms appear, allowing for early treatment and possible prevention.
In normally developing mice, the autism-associated Foxp1 gene was activated earlier than previously believed. This occurred during the period when apical radial glia was beginning to expand in numbers and generate a subset of neurons found deep in the developing brain. Mice lacking Foxp1 had fewer apical radial glia at the early stages of brain development.
No significant behavioral changes and no association with urinary beta-casomorphin concentrations were found in children on the autism spectrum who were fed a gluten-free or casein-free diet.