Recent data demonstrate a perceptual processing advantage for adult faces in both adults and young children, suggesting that face representation is shaped by visual experience accumulated with different face-age groups. As for species and race, this age bias may emerge during the first year of life as part of the general process of perceptual narrowing, given the extensive amount of social and perceptual experience accumulated with caregivers and/or other adult individuals. Using infant-controlled habituation and visual-paired comparison at test, two experiments were carried out to examine 3- and 9-month-olds' ability to discriminate within adult and infant faces. Results showed that, when they are provided with adequate time to visually compare the stimuli during test trials (Experiment 2), 3-month-olds exhibit above-chance discrimination of adult and infant faces. Instead, 9-month-olds discriminate adult faces but not infant faces (Experiments 1 and 2). Results provide the first evidence of age-related face processing biases in infancy, and show that by 9 months face representations tune to adult human faces.

Developmental dyslexia (DD) is a heritable neurodevelopmental reading disorder that could arise from auditory, visual, and cross-modal integration deficits. A deletion in intron 2 of the DCDC2 gene (hereafter DCDC2d) increases the risk for DD and related phenotypes. In this study, first we report that illusory visual motion perception-specifically processed by the magnocellular-dorsal (M-D) stream-is impaired in children with DD compared with age-matched and reading-level controls. Second, we test for the specificity of the DCDC2d effects on the M-D stream. Children with DD and DCDC2d need significantly more contrast to process illusory motion relative to their counterpart without DCDC2d and to age-matched and reading-level controls. Irrespective of the genetic variant, children with DD perform normally in the parvocellular-ventral task. Finally, we find that DCDC2d is associated with the illusory motion perception also in adult normal readers, showing that the M-D deficit is a potential neurobiological risk factor of DD rather than a simple effect of reading disorder. Our findings demonstrate, for the first time, that a specific neurocognitive dysfunction tapping the M-D stream is linked with a well-defined genetic susceptibility.

Rapid facial reactions (RFRs) to observed emotional expressions are proposed to be involved in a wide array of socioemotional skills, from empathy to social communication. Two of the most persuasive theoretical accounts propose RFRs to rely either on motor resonance mechanisms or on more complex mechanisms involving affective processes. Previous studies demonstrated that presentation of facial and bodily expressions can generate rapid changes in adult and school-age children's muscle activity. However, to date there is little to no evidence to suggest the existence of emotional RFRs from infancy to preschool age. To investigate whether RFRs are driven by motor mimicry or could also be a result of emotional appraisal processes, we recorded facial electromyographic (EMG) activation from the zygomaticus major and frontalis medialis muscles to presentation of static facial and bodily expressions of emotions (i.e., happiness, anger, fear, and neutral) in 3-year-old children. Results showed no specific EMG activation in response to bodily emotion expressions. However, observing others' happy faces led to increased activation of the zygomaticus major and decreased activation of the frontalis medialis, whereas observing others' angry faces elicited the opposite pattern of activation. This study suggests that RFRs are the result of complex mechanisms in which both affective processes and motor resonance may play an important role.

While the genetic and environmental contributions to developmental dyslexia (DD) have been studied extensively, the effects of identified genetic risk susceptibility and of specified environmental hazardous factors have usually been investigated separately. We assessed potential gene-by-environment (GxE) interactions on DD-related reading, spelling and memory phenotypes. The presence of GxE effects were investigated for the DYX1C1, DCDC2, KIAA0319 and ROBO1 genes, and for seven specified environmental moderators in 165 nuclear families in which at least one member had DD, by implementing a general test for GxE interaction in sib-pair-based association analysis of quantitative traits. Our results support a diathesis-stress model for both reading and memory composites: GxE effects were found between some specified environmental moderators (i.e. maternal smoke during pregnancy, birth weight and socio-economic status) and the DYX1C1-1259C/G marker. We have provided initial evidence that the joint analysis of identified genetic risk susceptibility and measured putative risk factors can be exploited in the study of the etiology of DD and reading-related neuropsychological phenotypes, and may assist in identifying/preventing the occurrence of DD.

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