Research using the intermodal preferential looking paradigm (IPLP) has consistently shown that English‐learning children aged 2 can associate transitive argument structure with causal events. However, studies using the same methodology investigating 2‐year‐old children’s knowledge of the conjoined agent intransitive and semantic role assignment have reported inconsistent findings. The aim of the present study was to establish at what age English‐learning children have verb‐general knowledge of both transitive and intransitive argument structure using a new method: the forced‐choice pointing paradigm. The results (...) suggest that young 2‐year‐olds can associate transitive structures with causal (or externally caused) events and can use transitive structure to assign agent and patient roles correctly. However, the children were unable to associate the conjoined agent intransitive with noncausal events until aged 3;4. The results confirm the pattern from previous IPLP studies and indicate that children may develop the ability to comprehend different aspects of argument structure at different ages. The implications for theories of language acquisition and the nature of the language acquisition mechanism are discussed. (shrink)

Executive functions (EFs) and impulsivity are dimensions of self-regulation that are both related to psychopathology. However, self-report measures of impulsivity and laboratory EF tasks typically display small correlations, and existing research indicates that impulsivity and EFs may tap separate aspects of self-regulation that independently statistically predict psychopathology in adulthood. However, relationships between EFs, impulsivity, and psychopathology may be different in childhood compared to adulthood. Here, we examine whether these patterns hold in the baseline assessment of the Adolescent Brain and Cognitive (...) Development (ABCD) sample, a national sample of over 11,000 children (including 749 twin pairs) ages 9–10 years. We examine the phenotypic and genetic relationships among latent variables for different components of EFs and multiple facets of impulsivity. Additionally, we assess how EFs and impulsivity relate to composite measures and latent variables of psychopathology derived from parent report. EFs were weakly correlated with impulsivity, and the strength varied by impulsivity facet, emphasizing their separability. We did not identify significant genetic and environmental correlations between EFs and impulsivity. Moreover, controlling for their small relationships with each other, both EFs and some facets of impulsivity statistically predicted an Externalizing factor, attention problems, and social problems, and twin analyses suggested these relationships were genetic in origin. These findings indicate that EFs and impulsivity represent phenotypically and genetically separable aspects of self-regulation that are both transdiagnostic correlates of psychopathology in childhood. (shrink)

We have shown that FEF lesion-induced extinction could be compensated for by changing the relative temporal onsets of two targets presented on either side of the midline. Monkeys were trained to make saccades to either of two identical visual stimuli presented with various stimulus onset asynchronies (SOA). In intact animals the targets were chosen with equal probability when they appeared simultaneously. After unilateral FEF lesions an SOA of 67–116 msec had to be introduced, with the contralesional target appearing first, to (...) obtain equal probability choice. With a smaller target separation, averaging saccades occurred with highest frequency at similar SOAs. Our findings suggest that neglect may be attributable to more time being required in the damaged hemisphere for converting sensory information into motor responses. (shrink)

The World Health Organisation recently listed air pollution as the most significant threat to human health. Air pollution comprises particulate matter (PM), metals, black carbon and gases such as ozone (O3), nitrogen dioxide (NO2) and carbon monoxide (CO). In addition to respiratory and cardiovascular disease, PM exposure is linked with increased risk of neurodegeneration as well as neurodevelopmental impairments. Critically, studies suggest that PM crosses the placenta, making direct in utero exposure a reality. Rodent models reveal that neuroinflammation, neurotransmitter imbalance (...) and oxidative stress are triggered following gestational/early life exposure to PM, and may be exacerbated by concomitant mitochondrial dysfunction. Gestational PM exposure (potentiated by mitochondrial impairment in the metabolically active neonatal brain) not only impacts neurodevelopment but may sensitise the brain to subsequent cognitive impairment. Having reviewed this field, we conclude that strategies are urgently required to reduce exposure to PM during this sensitive developmental period. (shrink)