1. Caulfield F, Ewing L, Burton N, Avard E, Rhodes G. {{Facial Trustworthiness Judgments in Children with ASD Are Modulated by Happy and Angry Emotional Cues}}. {PLoS One};2014;9(5):e97644.
Appearance-based trustworthiness inferences may reflect the misinterpretation of emotional expression cues. Children and adults typically perceive faces that look happy to be relatively trustworthy and those that look angry to be relatively untrustworthy. Given reports of atypical expression perception in children with Autism Spectrum Disorder (ASD), the current study aimed to determine whether the modulation of trustworthiness judgments by emotional expression cues in children with ASD is also atypical. Cognitively-able children with and without ASD, aged 6-12 years, rated the trustworthiness of faces showing happy, angry and neutral expressions. Trust judgments in children with ASD were significantly modulated by overt happy and angry expressions, like those of typically-developing children. Furthermore, subtle emotion cues in neutral faces also influenced trust ratings of the children in both groups. These findings support a powerful influence of emotion cues on perceived trustworthiness, which even extends to children with social cognitive impairments.
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2. Chan JS, Naumer MJ. {{Explaining autism spectrum disorders: central coherence versus predictive coding theories}}. {J Neurophysiol};2014 (May 28)
In this article, we review the paper Multisensory Temporal Integration in Autism Spectrum Disorders, by Stevenson et al. (2014). This paper illustrates the need to present different forms of stimuli in order to characterize the perceptual abilities of people with autism spectrum disorder (ASD). Furthermore, we will discuss their behavioral results and offer an opposing viewpoint to the suggested neuronal drivers of ASD.
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3. Chomiak T, Hung J, Cihal A, Dhaliwal J, Baghdadwala MI, Dzwonek A, Podgorny P, Hu B. {{Auditory-cued sensorimotor task reveals disengagement deficits in rats exposed to the autism-associated teratogen valproic acid}}. {Neuroscience};2014 (May 30);268:212-220.
Autism Spectrum Disorder (ASD) is often found to co-exist with non-core behavioral manifestations that include difficulties in disengagement of attention to sensory cues. Here we examined whether this behavioral abnormality can be induced in rats prenatally exposed to valproic acid (VPA), a well-established teratogen associated with ASD animal models. We tested rats using an auditory-cued sensorimotor task (ACST) based on the premise that ACST will be more sensitive to developmental changes in temporal association cortex (TeA) of the posterior attention system. We show that VPA rats learned the ACST markedly faster than control animals, but they exhibited a profound preoccupation with cues associated with the expectancy at the reward location such that disengagement was disrupted. Control rats on the other hand were able to disengage and utilize auditory cues for re-engagement. However, both control and VPA-treated rats performed similarly when tested on novel object recognition (NOR) and novel context mismatch (NOCM) behavioral tasks that are known to be sensitive to normal perirhinal and prefrontal network functioning respectively. Consistent with disrupted posterior rather than frontal networks, we also report that VPA can selectively act on deep-layer TeA cortical neurons by showing that VPA increased dendritic density in isolated deep-layer TeA but not frontal neurons. These results describe a useful approach to examine the role of cue-dependent control of attention systems in rodent models of autism and suggest that disengagement impairments may arise from an inability to modify behavior through the appropriate use of sensory cue associations.
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4. Dickinson A, Jones M, Milne E. {{Oblique Orientation Discrimination Thresholds Are Superior in Those with a High Level of Autistic Traits}}. {J Autism Dev Disord};2014 (May 29)
Enhanced low-level perception, although present in individuals with autism, is not seen in individuals with high, but non-clinical, levels of autistic traits (Brock et al.in Percept Lond 40(6):739. doi: 10.1068/p6953 , 2011). This is surprising, as many of the higher-level visual differences found in autism have been shown to correlate with autistic traits in non-clinical samples. Here we measure vertical-oblique and, more difficult, oblique-oblique orientation discrimination thresholds in a non-clinical sample. As predicted, oblique-oblique thresholds provided a more sensitive test of orientation discrimination, and were negatively related to autistic traits (N = 94, r = -.356, p < .0001). We conclude that individual differences in orientation discrimination and autistic traits are related, and suggest that both of these factors could be mediated by increased levels of the inhibitory neurotransmitter GABA.
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5. Dvash J, Ben-Zeev A, Noga A, Shamay-Tsoory S. {{The road not taken: social vs. private comparisons in Aspergers syndrome and high functioning autism}}. {Psychiatry Res};2014 (May 30);216(3):385-390.
Evaluation of the outcomes of our decisions may instigate comparisons of our actual outcome with those of others (social comparisons) or comparisons with alternative outcomes of choices not made (private comparisons). Previous research has suggested a deficit in attention to social information among individuals with autism spectrum disorders. As social comparison involves the processing of social information, here we investigated the orientation towards and sensitivity to social vs. private comparisons in individuals with autism spectrum disorders. We compared the sensitivity to social vs. private comparisons among individuals diagnosed with Asperger’s Syndrome (AS) or High Functioning Autism, using a task that entailed monetary rewards. Results showed that while individuals with AS generally demonstrate comparable sensitivity to absolute and relative rewards, they show less sensitivity to social comparison as compared to controls. Furthermore, they are characterized by a higher sensitivity to private rather than social comparison. These results suggest that low sensitivity to social comparisons is an important factor to consider in autism spectrum disorders.
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6. Frye RE. {{Clinical potential, safety, and tolerability of arbaclofen in the treatment of autism spectrum disorder}}. {Drug Healthc Patient Saf};2014;6:69-76.
Autism spectrum disorder (ASD) is a behaviorally defined disorder which has increased in prevalence over the last two decades. Despite decades of research, no effective treatment is currently available. Animal models, as well as other lines of evidence, point to abnormalities in the balance of cortical excitation to inhibition in individuals with ASD, with this imbalance resulting in an overall increase in cortical excitation. To reduce cortical excitatory glutamate pathways, arbaclofen, a selective agonist of the gamma aminobutyric acid receptor type B, has been developed. This article reviews the evidence for this treatment for ASD using a systematic review methodology. Overall, a systematic search of the literature revealed 148 relevant references with the majority of these being review papers or news items that mentioned the potential promise of arbaclofen. Five original studies were identified, four of which used STX209, a form of arbaclofen developed by Seaside Therapeutics, Inc., and one which used R-baclofen. In an animal model, treatment of Fragile X, a genetic disease with ASD features, demonstrated a reversal of behavioral, neurological, and neuropathological features associated with the disease. One double-blind, placebo-controlled study treated children and adults with Fragile X. Results from this study were promising, with signs of improvement in social function, especially in the most severely socially impaired. Two studies, one open-label and one double-blind, placebo-controlled, were conducted in children, adolescents, and young adults with ASD. These studies suggested some improvements in socialization, although the effects were limited and may have been driven by individuals with ASD that were higher-functioning. These studies and others that have used arbaclofen for the treatment of gastroesophageal reflux suggest that arbaclofen is safe and well-tolerated. Clearly, further clinical studies are needed in order to refine the symptoms and characteristics of children with ASD that are best treated with arbaclofen.
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7. Jackson JB, Roper SO. {{Parental Adaptation to Out-of-Home Placement of a Child With Severe or Profound Developmental Disabilities}}. {Am J Intellect Dev Disabil};2014 (May);119(3):203-219.
Abstract Utilizing grounded theory qualitative research methods, a model was developed for describing parental adaptation after voluntary placement of a child with severe or profound developmental disabilities in out-of-home care. Interviews of parents from 20 families were analyzed. Parents’ cognitive appraisals of placement outcomes were classified as either inducing emotional stress (i.e., guilt, sadness, fear and worry, anger and frustration, and uncertainty) or relief. Parental appraisals of responses to placement by children, extended family, and friends were identified as factors affecting the parents’ adaptation to placement. The primary coping methods used by parents to decrease emotional stress and increase relief consisted of reappraisals regarding the necessity of placement, involvement in the child’s life, psychotherapy, and the passage of time.
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8. Janusonis S. {{Serotonin dynamics in and around the central nervous system: Is autism solvable without fundamental insights?}}. {Int J Dev Neurosci};2014 (May 30)
Altered serotonin (5-hydroxytryptamine, 5-HT) signaling has been implicated in some developmental abnormalities of autism spectrum disorder (ASD). However, the presumed role of 5-HT in ASD raises new questions in fundamental neuroscience. Specifically, it is not clear if the current piecemeal approach to 5-HT signaling in the mammalian body is effective and whether new conceptual approaches may be required. This review briefly discusses 5-HT production and circulation in the central nervous system and outside of it, especially with regard to ASD, and proposes a more encompassing approach that questions the utility of the « neurotransmitter » concept. It then introduces the idea of a generalized 5-HT packet that may offer insights into possible links between serotonergic varicosities and blood platelets. These approaches have theoretical significance, but they are also well positioned to advance our understanding of some long-standing problems in autism research.
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9. Jiang YH, Wang Y, Xiu X, Choy KW, Pursley AN, Cheung SW. {{Genetic diagnosis of autism spectrum disorders: The opportunity and challenge in the genomics era}}. {Crit Rev Clin Lab Sci};2014 (May 30):1-14.
Abstract A genetic etiology for autism spectrum disorders (ASDs) was first suggested from twin studies reported in the 1970s. The identification of gene mutations in syndromic ASDs provided evidence to support a genetic cause of ASDs. More recently, genome-wide copy number variant and sequence analyses have uncovered a list of rare and highly penetrant copy number variants (CNVs) or single nucleotide variants (SNVs) associated with ASDs, which has strengthened the claim of a genetic etiology for ASDs. Findings from research studies in the genetics of ASD now support an important role for molecular diagnostics in the clinical genetics evaluation of ASDs. Various molecular diagnostic assays including single gene tests, targeted multiple gene panels and copy number analysis should all be considered in the clinical genetics evaluation of ASDs. Whole exome sequencing could also be considered in selected clinical cases. However, the challenge that remains is to determine the causal role of genetic variants identified through molecular testing. Variable expressivity, pleiotropic effects and incomplete penetrance associated with CNVs and SNVs also present significant challenges for genetic counseling and prenatal diagnosis.
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10. Murphy CM, Christakou A, Daly EM, Ecker C, Giampietro V, Brammer M, Smith AB, Johnston P, Robertson DM, Murphy DG, Rubia K. {{Abnormal Functional Activation and Maturation of Fronto-Striato-Temporal and Cerebellar Regions During Sustained Attention in Autism Spectrum Disorder}}. {Am J Psychiatry};2014 (May 30)
OBJECTIVE Sustained attention problems are common in people with autism spectrum disorder (ASD) and may have significant implications for the diagnosis and management of ASD and associated comorbidities. Furthermore, ASD has been associated with atypical structural brain development. The authors used functional MRI to investigate the functional brain maturation of attention between childhood and adulthood in people with ASD. METHOD Using a parametrically modulated sustained attention/vigilance task, the authors examined brain activation and its linear correlation with age between childhood and adulthood in 46 healthy male adolescents and adults (ages 11-35 years) with ASD and 44 age- and IQ-matched typically developing comparison subjects. RESULTS Relative to the comparison group, the ASD group had significantly poorer task performance and significantly lower activation in inferior prefrontal cortical, medial prefrontal cortical, striato-thalamic, and lateral cerebellar regions. A conjunction analysis of this analysis with group differences in brain-age correlations showed that the comparison group, but not the ASD group, had significantly progressively increased activation with age in these regions between childhood and adulthood, suggesting abnormal functional brain maturation in ASD. Several regions that showed both abnormal activation and functional maturation were associated with poorer task performance and clinical measures of ASD and inattention. CONCLUSIONS The results provide first evidence that abnormalities in sustained attention networks in individuals with ASD are associated with underlying abnormalities in the functional brain maturation of these networks between late childhood and adulthood.
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11. Nickl-Jockschat T, Rottschy C, Thommes J, Schneider F, Laird AR, Fox PT, Eickhoff SB. {{Neural networks related to dysfunctional face processing in autism spectrum disorder}}. {Brain Struct Funct};2014 (May 29)
One of the most consistent neuropsychological findings in autism spectrum disorders (ASD) is a reduced interest in and impaired processing of human faces. We conducted an activation likelihood estimation meta-analysis on 14 functional imaging studies on neural correlates of face processing enrolling a total of 164 ASD patients. Subsequently, normative whole-brain functional connectivity maps for the identified regions of significant convergence were computed for the task-independent (resting-state) and task-dependent (co-activations) state in healthy subjects. Quantitative functional decoding was performed by reference to the BrainMap database. Finally, we examined the overlap of the delineated network with the results of a previous meta-analysis on structural abnormalities in ASD as well as with brain regions involved in human action observation/imitation. We found a single cluster in the left fusiform gyrus showing significantly reduced activation during face processing in ASD across all studies. Both task-dependent and task-independent analyses indicated significant functional connectivity of this region with the temporo-occipital and lateral occipital cortex, the inferior frontal and parietal cortices, the thalamus and the amygdala. Quantitative reverse inference then indicated an association of these regions mainly with face processing, affective processing, and language-related tasks. Moreover, we found that the cortex in the region of right area V5 displaying structural changes in ASD patients showed consistent connectivity with the region showing aberrant responses in the context of face processing. Finally, this network was also implicated in the human action observation/imitation network. In summary, our findings thus suggest a functionally and structurally disturbed network of occipital regions related primarily to face (but potentially also language) processing, which interact with inferior frontal as well as limbic regions and may be the core of aberrant face processing and reduced interest in faces in ASD.
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12. Yang JC, Niu YQ, Simon C, Seritan AL, Chen L, Schneider A, Moghaddam ST, Hagerman PJ, Hagerman RJ, Olichney JM. {{Memantine Effects on Verbal Memory in Fragile X-associated Tremor/Ataxia Syndrome (FXTAS): a Double-blind Brain Potential Study}}. {Neuropsychopharmacology};2014 (May 29)
Older FMR1 premutation carriers may develop fragile X-associated tremor/ataxia syndrome (FXTAS), a neurodegenerative disorder manifesting cognitive deficits that often subsequently progress to dementia. To date, there is no specific treatment available for FXTAS. Studies have demonstrated the premutation associated overactivation of glutamatergic receptors in neurons. Memantine, a NMDA receptor antagonist approved for treatment of Alzheimer’s disease, thus was tested in the first placebo-controlled, double-blind, randomized clinical trial in FXTAS. Prior event-related brain potential (ERP) studies in FXTAS found reduced N400 repetition effect, a glutamate-related electrophysiological marker of semantic priming and verbal memory processes. This substudy of the randomized clinical trial of memantine in FXTAS sought to use the N400 repetition effect to evaluate effects of chronic memantine treatment on verbal memory. Subsequent recall and recognition memory tests for the experimental stimuli were administered to characterize verbal memory. Data from 41 patients who completed the 1 year memantine trial (21 on memantine) and also completed longitudinal ERP studies were analysed. Results showed treatment-associated benefits on both cued-recall memory and N400 repetition effect amplitude. Importantly, improvement in cued-recall was positively correlated with amplitude increase of the N400 repetition effect. The placebo group, in contrast, displayed a significant reduction of the N400 repetition effect after 1 year. These results suggest that memantine treatment may have beneficial effects on verbal memory in FXTAS. Additional studies of memantine, perhaps in combination with other therapeutic agents, appear warranted, as symptomatic treatments and neuroprotective treatments are both needed for this recently recognized neurodegenerative disorder.Neuropsychopharmacology accepted article preview online, 29 May 2014; doi:10.1038/npp.2014.122.
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13. Zen Y, Hirohata H, Yuge M, Watanabe Y. {{Results of an intervention to support adolescents with developmental disabilities through cooperation between the school and community health services The necessity for preventive measures for mental disorders in adolescents}}. {Nihon Koshu Eisei Zasshi};2014;61(5):212-220.
