1. {{Correction: are maternal social networks and perceptions of trust associated with suspected autism spectrum disorder in offspring? A population-based study in Japan}}. {PLoS One};2014;9(7):e104332.
[This corrects the article DOI: 10.1371/journal.pone.0101359.].
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2. Daly E, Ecker C, Hallahan B, Deeley Q, Craig M, Murphy C, Johnston P, Spain D, Gillan N, Gudbrandsen M, Brammer M, Giampietro V, Lamar M, Page L, Toal F, Schmitz N, Cleare A, Robertson D, Rubia K, Murphy DG. {{Response inhibition and serotonin in autism: a functional MRI study using acute tryptophan depletion}}. {Brain};2014 (Jul 28)
It has been suggested that the restricted, stereotyped and repetitive behaviours typically found in autism are underpinned by deficits of inhibitory control. The biological basis of this is unknown but may include differences in the modulatory role of neurotransmitters, such as serotonin, which are implicated in the condition. However, this has never been tested directly. We therefore assessed the modifying role of serotonin on inhibitory brain function during a Go/No-Go task in 14 adults with autism and normal intelligence and 14 control subjects that did not differ in gender, age and intelligence. We undertook a double-blind, placebo-controlled, crossover trial of acute tryptophan depletion using functional magnetic resonance imaging. Following sham, adults with autism relative to controls had reduced activation in key inhibitory regions of inferior frontal cortex and thalamus, but increased activation of caudate and cerebellum. However, brain activation was modulated in opposite ways by depletion in each group. Within autistic individuals depletion upregulated fronto-thalamic activations and downregulated striato-cerebellar activations toward control sham levels, completely ‘normalizing’ the fronto-cerebellar dysfunctions. The opposite pattern occurred in controls. Moreover, the severity of autism was related to the degree of differential modulation by depletion within frontal, striatal and thalamic regions. Our findings demonstrate that individuals with autism have abnormal inhibitory networks, and that serotonin has a differential, opposite, effect on them in adults with and without autism. Together these factors may partially explain the severity of autistic behaviours and/or provide a novel (tractable) treatment target.
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3. Klaiman C, Quintin EM, Jo B, Lightbody AA, Hazlett HC, Piven J, Hall SS, Reiss AL. {{Longitudinal Profiles of Adaptive Behavior in Fragile X Syndrome}}. {Pediatrics};2014 (Jul 28)
OBJECTIVE: To examine longitudinally the adaptive behavior patterns in fragile X syndrome. METHOD: Caregivers of 275 children and adolescents with fragile X syndrome and 225 typically developing children and adolescents (2-18 years) were interviewed with the Vineland Adaptive Behavior Scales every 2 to 4 years as part of a prospective longitudinal study. RESULTS: Standard scores of adaptive behavior in people with fragile X syndrome are marked by a significant decline over time in all domains for males and in communication for females. Socialization skills are a relative strength as compared with the other domains for males with fragile X syndrome. Females with fragile X syndrome did not show a discernible pattern of developmental strengths and weaknesses. CONCLUSIONS: This is the first large-scale longitudinal study to show that the acquisition of adaptive behavior slows as individuals with fragile X syndrome age. It is imperative to ensure that assessments of adaptive behavior skills are part of intervention programs focusing on childhood and adolescence in this condition.
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4. McMahon CM, Henderson HA. {{Error-monitoring in response to social stimuli in individuals with higher-functioning Autism Spectrum Disorder}}. {Dev Sci};2014 (Jul 28)
Error-monitoring, or the ability to recognize one’s mistakes and implement behavioral changes to prevent further mistakes, may be impaired in individuals with Autism Spectrum Disorder (ASD). Children and adolescents (ages 9-19) with ASD (n = 42) and typical development (n = 42) completed two face processing tasks that required discrimination of either the gender or affect of standardized face stimuli. Post-error slowing and the difference in Error-Related Negativity amplitude between correct and incorrect responses (ERNdiff ) were used to index error-monitoring ability. Overall, ERNdiff increased with age. On the Gender Task, individuals with ASD had a smaller ERNdiff than individuals with typical development; however, on the Affect Task, there were no significant diagnostic group differences on ERNdiff . Individuals with ASD may have ERN amplitudes similar to those observed in individuals with typical development in more social contexts compared to less social contexts due to greater consequences for errors, more effortful processing, and/or reduced processing efficiency in these contexts. Across all participants, more post-error slowing on the Affect Task was associated with better social cognitive skills.
