1. Alaerts K, Swinnen SP, Wenderoth N. {{Neural processing of biological motion in autism: An investigation of brain activity and effective connectivity}}. {Sci Rep};2017 (Jul 17);7(1):5612.
The superior temporal sulcus (STS) forms a key region for social information processing and disruptions of its function have been associated with socio-communicative impairments characteristic of autism spectrum disorders (ASD). Task-based fMRI was applied in 15 adults with ASD and 15 matched typical-controls (TC) to explore differences in activity and effective connectivity of STS while discriminating either ‘intact’ versus ‘scrambled’ biological motion point light displays (explicit processing) or responding to a color-change while the ‘intact’ versus ‘scrambled’ nature of the stimulus was irrelevant for the task (implicit processing). STS responded stronger to ‘intact’ than ‘scrambled’ stimuli in both groups, indicating that the basic encoding of ‘biological’ versus ‘non-biological’ motion seems to be intact in ASD. Only in the TC-group however, explicit attention to the biological motion content induced an augmentation of STS-activity, which was not observed in the ASD-group. Overall, these findings suggest an inadequacy to recruit STS upon task demand in ASD, rather than a generalized alteration in STS neural processing. The importance of attention orienting for recruiting relevant neural resources was further underlined by the observation that connectivity between STS and medial prefrontal cortex (mPFC), a key region in attention regulation, effectively modulated STS-recruitment in the ASD-group.
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2. Belagodu AP, Fleming S, Galvez R. {{Neocortical developmental analysis of vasculature and their growth factors offer new insight into Fragile X Syndrome abnormalities}}. {Dev Neurobiol};2017 (Jul 18)
Fragile X Syndrome (FXS) is the most common single gene cause for Autism Spectrum Disorder and the most prevalent form of inherited mental retardation. Our prior studies have demonstrated that adult FXS mice have abnormal blood vessel density (BVD) and elevated Vascular Endothelial Growth Factor A expression (VEGF-A). VEGF-A is one of the most prominent regulators of BVD, and its abnormal expression is the most likely cause for FXS BVD abnormalities. We have demonstrated that attenuating elevated VEGF-A expression can ameliorate many non-vascular FXS abnormalities(Belagodu et al., 2017), suggesting that abnormal VEGF-A expression is an underlying cause for some FXS abnormalities. However, FXS is a developmental disorder and VEGF-A’s potential role in mediating FXS abnormalities during development have never been explored. Furthermore, VEGF-A is one protein in a family of proteins (VEGF-A, VEGF-B, VEGF-C, VEGF-D, & PLGF) that activate one of three primary receptors (VEGFR1, VEGFR2, & VEGFR3). Abnormal expression of any of these proteins could hinder proper development. The current study demonstrated that FXS mice do not exhibit normal BVD developmental patterns, resulting in elevated adult expression, most likely due to observed elevated VEGF-A adult expression. Interestingly, all five VEGF family of proteins exhibited altered developmental expression patterns that could cause abnormal development. However, none of the receptors exhibiting abnormal adult expression, but did exhibit altered developmental expression. Expanding upon our prior analyses, the current study provides additional interesting insight towards potential developmental mechanisms mediating FXS abnormalities, while offering further sites for age specific therapeutic interventions. This article is protected by copyright. All rights reserved.
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3. Craig AB, Grossman E, Krichmar JL. {{Investigation of autistic traits through strategic decision-making in games with adaptive agents}}. {Sci Rep};2017 (Jul 17);7(1):5533.
Autism Spectrum Disorders are characterized by difficulties in communicating and cooperating with other people. Impairment in Theory of Mind (ToM), the ability to infer what another person is thinking, may contribute to these social deficits. The present study assesses the relationship between autistic traits and decision-making in a socioeconomic game environment that measures ToM and cooperation. We quantified participant strategy during game play with computer agents that simulated aspects of ToM or fixed strategy agents with static behaviors or heuristics. Individuals with higher Autism Quotient (AQ) scores cooperated less than subjects with low AQ scores with the ToM agents. In contrast, subjects with higher AQ scores cooperated more with fixed strategy agents. Additionally, subjects with higher AQ scores spent more time than low AQ subjects signaling cooperative intent in games with fixed strategy agents while spending less time signaling cooperation with adaptive agents, indicating a preference toward systemizing behaviors in the face of uncertainty. We conclude that individuals with high levels of autistic traits are less likely to utilize ToM as a cognitive strategy, even when it is beneficial, to achieve a desired outcome.
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4. Hatfield M, Murray N, Ciccarelli M, Falkmer T, Falkmer M. {{Pilot of the BOOST-A: An online transition planning program for adolescents with autism}}. {Aust Occup Ther J};2017 (Jul 19)
BACKGROUND: Many adolescents with autism face difficulties with the transition from high school into post-school activities. The Better OutcOmes & Successful Transitions for Autism (BOOST-A) is an online transition planning program which supports adolescents on the autism spectrum to prepare for leaving school. This study describes the development of the BOOST-A and aimed to determine the feasibility and viability of the program. METHODS: Two pilot studies were conducted. In Pilot A, the BOOST-A was trialled by six adolescents on the autism spectrum, their parents, and the professionals who worked with them, to determine its feasibility. In Pilot B, 88 allied health professionals (occupational therapists, speech pathologists, and psychologists) reviewed the BOOST-A to determine its viability. RESULTS: Participants rated the BOOST-A as a feasible tool for transition planning. The majority of allied health professionals agreed that it was a viable program. Based on participant feedback, the BOOST-A was modified to improve usability and feasibility. CONCLUSION: The BOOST-A is a viable and feasible program that has the potential to assist adolescents with autism in preparing for transitioning out of high school. Future research will determine the effectiveness of the BOOST-A with adolescents across Australia.
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5. Moazen-Zadeh E, Shirzad F, Karkhaneh-Yousefi MA, Khezri R, Mohammadi MR, Akhondzadeh S. {{Simvastatin as an Adjunctive Therapy to Risperidone in Treatment of Autism: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial}}. {J Child Adolesc Psychopharmacol};2017 (Jul 18)
OBJECTIVES: Providing novel treatments for autism has been a subject of long-standing research. Based on etiopathological findings, we aim at assessing potential therapeutic effects of statins, here simvastatin, on autism symptoms for the first time. METHODS: In this randomized, double-blind, placebo-controlled, parallel-group 10-week clinical trial, 70 drug-free children aged 4 to 12 years old with diagnosis of autistic disorder based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, who had an Aberrant Behavior Checklist-Community (ABC-C) scale irritability subscale score of >/=12, were equally randomized to receive either simvastatin (20-40 mg/day) or placebo as an adjunct to risperidone (1-2 mg/day) whereas administration of both drugs was started simultaneously from baseline. Patients with comorbid psychiatric disorders, active medical conditions, severe intellectual disability, seizure disorders, history of any treatments for autism in the past 6 months, or history of current anti-inflammatory drug consumption were excluded. Primary outcome was defined as the difference in mean change of the ABC-C scale irritability subscale score from baseline to the endpoint ( www.irct.ir ; IRCT201602041556N86). RESULTS: Significant differences in change of the ABC-C scale irritability (mean difference [95% confidence interval (CI)] = -3.45 [-5.37 to -1.54], p = 0.001; Cohen’s d = 0.89) and hyperactivity/noncompliance (mean difference [95% CI] = -4.27 [-6.69 to -1.86], p = 0.001; Cohen’s d = 0.87) subscales scores were detected between the two arms. No significant difference was detected in case of the other three subscales. CONCLUSIONS: This study provides preliminary evidence for potential therapeutic effects of simvastatin in the treatment of autism that warrants further investigations.
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6. Rajan-Babu IS, Lian M, Cheah FSH, Chen M, Tan ASC, Prasath EB, Loh SF, Chong SS. {{FMR1 CGG repeat expansion mutation detection and linked haplotype analysis for reliable and accurate preimplantation genetic diagnosis of fragile X syndrome}}. {Expert Rev Mol Med};2017 (Jul 19);19:e10.
Fragile X mental retardation 1 (FMR1) full-mutation expansion causes fragile X syndrome. Trans-generational fragile X syndrome transmission can be avoided by preimplantation genetic diagnosis (PGD). We describe a robust PGD strategy that can be applied to virtually any couple at risk of transmitting fragile X syndrome. This novel strategy utilises whole-genome amplification, followed by triplet-primed polymerase chain reaction (TP-PCR) for robust detection of expanded FMR1 alleles, in parallel with linked multi-marker haplotype analysis of 13 highly polymorphic microsatellite markers located within 1 Mb of the FMR1 CGG repeat, and the AMELX/Y dimorphism for gender identification. The assay was optimised and validated on single lymphoblasts isolated from fragile X reference cell lines, and applied to a simulated PGD case and a clinical in vitro fertilisation (IVF)-PGD case. In the simulated PGD case, definitive diagnosis of the expected results was achieved for all ’embryos’. In the clinical IVF-PGD case, delivery of a healthy baby girl was achieved after transfer of an expansion-negative blastocyst. FMR1 TP-PCR reliably detects presence of expansion mutations and obviates reliance on informative normal alleles for determining expansion status in female embryos. Together with multi-marker haplotyping and gender determination, misdiagnosis and diagnostic ambiguity due to allele dropout is minimised, and couple-specific assay customisation can be avoided.
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7. Rhodes G, Burton N, Jeffery L, Read A, Taylor L, Ewing L. {{Facial expression coding in children and adolescents with autism: Reduced adaptability but intact norm-based coding}}. {Br J Psychol};2017 (Jul 19)
Individuals with autism spectrum disorder (ASD) can have difficulty recognizing emotional expressions. Here, we asked whether the underlying perceptual coding of expression is disrupted. Typical individuals code expression relative to a perceptual (average) norm that is continuously updated by experience. This adaptability of face-coding mechanisms has been linked to performance on various face tasks. We used an adaptation aftereffect paradigm to characterize expression coding in children and adolescents with autism. We asked whether face expression coding is less adaptable in autism and whether there is any fundamental disruption of norm-based coding. If expression coding is norm-based, then the face aftereffects should increase with adaptor expression strength (distance from the average expression). We observed this pattern in both autistic and typically developing participants, suggesting that norm-based coding is fundamentally intact in autism. Critically, however, expression aftereffects were reduced in the autism group, indicating that expression-coding mechanisms are less readily tuned by experience. Reduced adaptability has also been reported for coding of face identity and gaze direction. Thus, there appears to be a pervasive lack of adaptability in face-coding mechanisms in autism, which could contribute to face processing and broader social difficulties in the disorder.
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8. Saghazadeh A, Rezaei N. {{Systematic review and meta-analysis links autism and toxic metals and highlights the impact of country development status: Higher blood and erythrocyte levels for mercury and lead, and higher hair antimony, cadmium, lead, and mercury}}. {Prog Neuropsychopharmacol Biol Psychiatry};2017 (Jul 14)
BACKGROUND: Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental disorder that affects cognitive and higher cognitive functions. Increasing prevalence of ASD and high rates of related comorbidities has caused serious health loss and placed an onerous burden on the supporting families, caregivers, and health care services. Heavy metals are among environmental factors that may contribute to ASD. However, due to inconsistencies across studies, it is still hard to explain the association between ASD and toxic metals. Therefore the objective of this study was to investigate the difference in heavy metal measures between patients with ASD and control subjects. METHODS: We included observational studies that measured levels of toxic metals (antimony, arsenic, cadmium, lead, manganese, mercury, nickel, silver, and thallium) in different specimens (whole blood, plasma, serum, red cells, hair and urine) for patients with ASD and for controls. The main electronic medical database (PubMed and Scopus) were searched from inception through October 2016. RESULTS: 52 studies were eligible to be included in the present systematic review, of which 48 studies were included in the meta-analyses. The hair concentrations of antimony (standardized mean difference (SMD)=0.24; 95% confidence interval (CI): 0.03 to 0.45) and lead (SMD=0.60; 95% confidence interval (CI): 0.17 to 1.03) in ASD patients were significantly higher than those of control subjects. ASD patients had higher erythrocyte levels of lead (SMD=1.55, CI: 0.2 to 2.89) and mercury (SMD=1.56, CI: 0.42 to 2.70). There were significantly higher blood lead levels in ASD patients (SMD=0.43, CI: 0.02 to 0.85). Sensitivity analyses showed that ASD patients in developed but not in developing countries have lower hair concentrations of cadmium (SMD=-0.29, CI: -0.46 to -0.12). Also, such analyses indicated that ASD patients in developing but not in developed lands have higher hair concentrations of lead (SMD=1.58, CI: 0.80 to 2.36) and mercury (SMD=0.77, CI: 0.31 to 1.23). These findings were confirmed by meta-regression analyses indicating that development status of countries significantly influences the overall effect size of mean difference for hair arsenic, cadmium, lead, and mercury between patients with ASD and controls. CONCLUSION: The findings help highlighting the role of toxic metals as environmental factors in the etiology of ASD, especially in developing lands. While there are environmental factors other than toxic metals that greatly contribute to the etiology of ASD in developed lands. It would be, thus, expected that classification of ASD includes etiological entities of ASD on the basis of implication of industrial pollutants (developed vs. developing ASD).
