"Autism spectrum disorders (henceforth autism) are diagnosed in around 1% of the population [1]. Familial liability confers risk for a broad spectrum of difficulties including the broader autism phenotype (BAP) [2, 3]. There are currently no reliable predictors of autism in infancy, but characteristic behaviors emerge during the second year, enabling diagnosis after this age [4, 5]. Because indicators of brain functioning may be sensitive predictors, and atypical eye contact is characteristic of the syndrome [6-9] and the BAP [10, 11], we examined whether neural sensitivity to eye gaze during infancy is associated with later autism outcomes [12, 13]. We undertook a prospective longitudinal study of infants with and without familial risk for autism. At 6-10 months, we recorded infants' event-related potentials (ERPs) in response to viewing faces with eye gaze directed toward versus away from the infant [14]. Longitudinal analyses showed that characteristics of ERP components evoked in response to dynamic eye gaze shifts during infancy were associated with autism diagnosed at 36 months. ERP responses to eye gaze may help characterize developmental processes that lead to later emerging autism. Findings also elucidate the mechanisms driving the development of the social brain in infancy."
"The current study investigated early temperament in 54 infants at familial high-risk of ASD and 50 controls. Parental report of temperament was assessed around 7, 14 and 24 months of age and diagnostic assessment was conducted at 3 years. The high-risk group showed reduced Surgency at 7 and 14 months and reduced Effortful Control at 14 and 24 months, compared to controls. High-risk infants later diagnosed with ASD were distinguished from controls by a temperament profile marked by increased Perceptual Sensitivity from the first year of life, and increased Negative Affect and reduced Cuddliness in the second year of life. Temperament may be an important construct for understanding the early infant development of ASD."
"Whilst joint attention (JA) impairments in autism have been widely studied, little is known about the early development of gaze following, a precursor to establishing JA. We employed eye-tracking to record gaze following longitudinally in infants with and without a family history of autism spectrum disorder (ASD) at 7 and 13 months. No group difference was found between at-risk and low-risk infants in gaze following behaviour at either age. However, despite following gaze successfully at 13 months, at-risk infants with later emerging socio-communication difficulties (both those with ASD and atypical development at 36 months of age) allocated less attention to the congruent object compared to typically developing at-risk siblings and low-risk controls. The findings suggest that the subtle emergence of difficulties in JA in infancy may be related to ASD and other atypical outcomes."
Co-authored by ASF grantee Nina Leezenbaum, this study found delayed visual and oral exploration of objects in infant siblings of children with autism that were not observed in infants with no family history.
Researchers uncover a connection between exposure to traffic-related pollutants and autism risk. Findings suggest children living in high pollution areas are 3 times more likely to have autism compared to those living in low pollution areas.
A large, prospective study found that children with and without ASD were developmentally similar at 6 months based on clinical tests. Lead author Dr. Rebecca Landa reported, “for those children who went on to develop autism, the earliest signs of atypical development were non-specific to autism, such as general communication or motor delay.”
Dr. Eric Courchesne recently published his work he previewed at this year's IMFAR in the "Journal of the American Academy of Child & Adolescent Psychiatry."
The mRNA expression abnormalities reliably observed in peripheral blood mononuclear cells, which are safely and easily assayed in infants, offer the first potential peripheral blood–based, early biomarker panel of risk for autism in infants and toddlers. Future work should verify these biomarkers and evaluate whether they may also serve as indirect indices of deviant molecular neural mechanisms in autism.
