1. Carlier S, Kurzeja N, Ducenne L, Pauwen N, Leys C, Delvenne V. {{Differential profiles of four groups of children referred to an autism diagnostic service in Belgium: Autism-specific hallmarks}}. {J Intellect Disabil}. 2017: 1744629517713516.
OBJECTIVE: This article aims at exploring distinctive hallmarks of autistic disorders compared to other groups presenting mimicking and/or overlapping conditions. METHOD: The exploratory study involved 196 children with autism, intellectual disability, language impairment and psycho-affective disorders previously referred to an autism diagnostic service. The autism discriminative tool (ADT), a behavioural checklist, was used to compile and analyse the children’s profiles based on the clinical information gathered during diagnostic assessments. All samples were compared and analysed separately according to the checklist’s four domains. RESULTS: Children with autism showed greater frequency and severity of impairments on the ADT’s social and communication categories. These children also differed from other groups in terms of specific rigid behaviours and high frequency of atypical sensory responses. CONCLUSIONS: Results illustrate the psychopathology of autism spectrum disorder suspected children referred to a specialized autism diagnostic service, doing so by providing us with specific clinical profiles.
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2. Cheng N, Alshammari F, Hughes E, Khanbabaei M, Rho JM. {{Dendritic overgrowth and elevated ERK signaling during neonatal development in a mouse model of autism}}. {PLoS One}. 2017; 12(6): e0179409.
Autism spectrum disorder (hereafter referred to as « ASD ») is a heterogeneous neurodevelopmental condition characterized by impaired social communication and interactions, and restricted, repetitive activities or interests. Alterations in network connectivity and memory function are frequently observed in autism patients, often involving the hippocampus. However, specific changes during early brain development leading to disrupted functioning remain largely unclear. Here, we investigated the development of dendritic arbor of hippocampal CA1 pyramidal neurons in the BTBR T+tf/J (BTBR) mouse model of autism. BTBR mice display the defining behavioural features of autism, and also exhibit impaired learning and memory. We found that compared to control C57BL/6J (B6) animals, the lengths of both apical and basal dendrites were significantly greater in neonatal BTBR animals. Further, basal dendrites in the BTBR mice had higher branching complexity. In contrast, cross-sectional area of the soma was unchanged. In addition, we observed a similar density of CA1 pyramidal neurons and thickness of the neuronal layer between the two strains. Thus, there was a specific, compartmentalized overgrowth of dendrites during early development in the BTBR animals. Biochemical analysis further showed that the extracellular signal-regulated kinases (ERK) pathway was up-regulated in the hippocampus of neonatal BTBR animals. Since dendritic structure is critical for information integration and relay, our data suggest that altered development of dendrites could potentially contribute to impaired hippocampal function and behavior observed in the BTBR model, and that this might be related to increased activation of the ERK pathway.
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3. Cuevas-Olguin R, Roychowdhury S, Banerjee A, Garcia-Oscos F, Esquivel-Rendon E, Bringas ME, Kilgard MP, Flores G, Atzori M. {{Cerebrolysin prevents deficits in social behavior, repetitive conduct, and synaptic inhibition in a rat model of autism}}. {J Neurosci Res}. 2017.
Autism spectrum disorder (ASD) is a syndrome of diverse neuropsychiatric diseases of growing incidence characterized by repetitive conduct and impaired social behavior and communication for which effective pharmacological treatment is still unavailable. While the mechanisms and etiology of ASD are still unknown, a consensus is emerging about the synaptic nature of the syndrome, suggesting a possible avenue for pharmacological treatment with synaptogenic compounds. The peptidic mixture cerebrolysin (CBL) has been successfully used during the last three decades in the treatment of stroke and neurodegenerative disease. Animal experiments indicate that at least one possible mechanism of action of CBL is through neuroprotection and/or synaptogenesis. In the present study, we tested the effect of CBL treatment (daily injection of 2.5 mL/Kg i.p. during 15 days) on a rat model of ASD. This was based on the offspring (43 male and 51 female pups) of a pregnant female rat injected with valproic acid (VPA, 600 mg/Kg) at the embryonic day 12.5, which previous work has shown to display extensive behavioral, as well as synaptic impairment. Comparison between saline vs. CBL-injected VPA animals shows that CBL treatment improves behavioral as well as synaptic impairments, measured by behavioral performance (social interaction, Y-maze, plus-maze), maximal response of inhibitory gamma-amino butyric acid type A receptor (GABAA R)-mediated synaptic currents, as well as their kinetic properties and adrenergic and muscarinic modulation. We speculate that CBL might be a viable and effective candidate for pharmacological treatment or co-treatment of ASD patients. (c) 2017 Wiley Periodicals, Inc.
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4. Freedman EG, Foxe JJ. {{Eye-movements, sensori-motor adaptation and cerebellar-dependent learning in Autism: Towards potential biomarkers and sub-phenotypes}}. {Eur J Neurosci}. 2017.
Because of the wide range of symptoms expressed in individuals with Autism Spectrum Disorder (ASD) and their idiosyncratic severity it is unlikely that a single remedial approach will be universally effective. Resolution of this dilemma requires identifying subgroups within the autism spectrum, based on symptom set and severity, on an underlying neuro-structural difference, and on specific behavioral dysfunction. This will provide critical insight into the disorder and may lead to better diagnoses, and more targeted remediation in these subphenotypes of people with ASD. In this review we discuss findings that appear to link the structure of the cerebellar vermis and plasticity of the saccadic eye movement system in people with an Autism Spectrum Disorder (ASD). Differences in cerebellar vermis structure in ASD could critically impact visuo-sensori-motor development in early infancy, which may in turn manifest as the visual orienting, communication and social interaction differences often seen in this population. It may be possible to distinguish a subpopulation of children with vermal hypoplasia, to establish whether this group manifests more severe deficits in visual orienting and in adaptation to persistent visual errors, and to establish whether this putative subphenotype of ASD is associated with a specific and distinct clinical symptom profile. This article is protected by copyright. All rights reserved.
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5. He CX, Cantu DA, Mantri SS, Zeiger WA, Goel A, Portera-Cailliau C. {{Tactile defensiveness and impaired adaptation of neuronal activity in the Fmr1 knockout mouse model of autism}}. {J Neurosci}. 2017.
Sensory hypersensitivity is a common symptom in autism spectrum disorders (ASDs), including Fragile X Syndrome (FXS), and frequently leads to tactile defensiveness. In mouse models of ASDs, there is mounting evidence of neuronal and circuit hyperexcitability in several brain regions, which could contribute to sensory hypersensitivity. However, it is not yet known whether or how sensory stimulation might trigger abnormal sensory processing at the circuit level or abnormal behavioral responses in ASD mouse models, especially during an early developmental time when experience-dependent plasticity shapes such circuits. Using a novel assay, we discovered exaggerated motor responses to whisker stimulation in young Fmr1 knockout (KO) mice (postnatal days (P) 14-16), a model of FXS. Adult Fmr1 KO mice actively avoided a stimulus that was innocuous to wild-type controls, a sign of tactile defensiveness. Using in vivo two-photon calcium imaging of Layer 2/3 barrel cortex neurons expressing GCaMP6s, we found no differences between wild-type and Fmr1 KO mice in overall whisker-evoked activity, though 45% fewer neurons in young Fmr1 KO mice responded in a time-locked manner. Notably, we identified a pronounced deficit in neuronal adaptation to repetitive whisker stimulation in both young and adult Fmr1 KO mice. Thus, impaired adaptation in cortical sensory circuits is a potential cause of tactile defensiveness in autism.SIGNIFICANCE STATEMENTWe use a novel paradigm of repetitive whisker stimulation and in vivo calcium imaging to assess tactile defensiveness and barrel cortex activity in young and adult Fmr1 knockout mice, the mouse model of Fragile X Syndrome. We describe evidence of tactile defensiveness, as well as a lack of L2/3 neuronal adaptation in barrel cortex, during whisker stimulation. We propose that a defect in sensory adaptation within local neuronal networks, beginning at a young age and continuing into adulthood, likely contributes to sensory overreactivity in FXS and perhaps other ASDs.
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6. Hornig M, Bresnahan MA, Che X, Schultz AF, Ukaigwe JE, Eddy ML, Hirtz D, Gunnes N, Lie KK, Magnus P, Mjaaland S, Reichborn-Kjennerud T, Schjolberg S, Oyen AS, Levin B, Susser ES, Stoltenberg C, Lipkin WI. {{Prenatal fever and autism risk}}. {Mol Psychiatry}. 2017.
Some studies suggest that prenatal infection increases risk of autism spectrum disorders (ASDs). This study was undertaken in a prospective cohort in Norway to examine whether we could find evidence to support an association of the prenatal occurrence of fever, a common manifestation of infection, with ASD risk. Prospective questionnaires provided maternal exposure data; case status was established from clinical assessments and registry linkages. In a large, prospectively ascertained cohort of pregnant mothers and their offspring, we examined infants born 32 weeks for associations between fever exposure in each trimester and ASD risk using logistic regression. Maternal exposure to second-trimester fever was associated with increased ASD risk, adjusting for presence of fever in other trimesters and confounders (adjusted odds ratio (aOR), 1.40; 95% confidence interval, 1.09-1.79), with a similar, but nonsignificant, point estimate in the first trimester. Risk increased markedly with exposure to three or more fever episodes after 12 weeks’ gestation (aOR, 3.12; 1.28-7.63). ASD risk appears to increase with maternal fever, particularly in the second trimester. Risk magnified dose dependently with exposure to multiple fevers after 12 weeks’ gestation. Our findings support a role for gestational maternal infection and innate immune responses to infection in the pathogenesis of at least some cases of ASD.Molecular Psychiatry advance online publication, 13 June 2017; doi:10.1038/mp.2017.119.
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7. Hsu CT, Neufeld J, Chakrabarti B. {{Reduced reward related neural response to mimicry in individuals with autism}}. {Eur J Neurosci}. 2017.
Mimicry is a facilitator of social bonds in humans, from infancy. This facilitation is made possible through changing the reward value of social stimuli, e.g. we like and affiliate more with people who mimic us. Autism Spectrum Disorders (ASD) are marked by difficulties in forming social bonds. In this study, we investigate whether the reward-related neural response to being mimicked is altered in individuals with ASD, using a simple conditioning paradigm. Multiple studies in humans and nonhuman primates have established a crucial role for the ventral striatal (VS) region in responding to rewards. In this study, adults with ASD and matched controls first underwent a conditioning task outside the scanner, where they were mimicked by one face and ‘anti-mimicked’ by another. In the second part, participants passively viewed the conditioned faces in a 3T MRI scanner using a multi-echo sequence. The differential neural response towards mimicking vs anti-mimicking faces in the VS was tested for group differences as well as an association with self-reported autistic traits. Multiple regression analysis revealed lower left VS response to mimicry [mimicking > anti-mimicking faces] in the ASD group compared to controls. The VS response to mimicry was negatively correlated with autistic traits across the whole sample. Our results suggest that for individuals with ASD and high autistic traits, being mimicked is associated with lower reward-related neural response. This result points to a potential mechanism underlying the difficulties reported by many of individuals with ASD in building social rapport. This article is protected by copyright. All rights reserved.
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8. Kaluzna-Czaplinska J, Jozwik-Pruska J, Chirumbolo S, Bjorklund G. {{Tryptophan status in autism spectrum disorder and the influence of supplementation on its level}}. {Metab Brain Dis}. 2017.
Recent reports show that the worldwide incidence of autism spectrum disorder (ASD) is dramatically increasing, although ASD etiology and pathogenesis are still far to be fully elucidated. Some dietary-derived essential compounds, such as the amino acid tryptophan, appear to be impaired in patients with ASD. Tryptophan (Trp) plays a significant role in the human organism and serves as a precursor for a wide range of bioactive compounds, including major neurotransmitters. Research indicates that tryptophan might be deficient in subjects with ASD. Deficiency in the tryptophan level can be retrieved by investigating Trp levels or its major metabolite kynurenine in urines. The purpose of the present study is to quantify tryptophan content in urine samples (n = 236) of ASD patients, who underwent a supplemented dietary panel with B vitamins and magnesium, compared to controls (without this diet regimen). The samples were analyzed with gas chromatography-mass spectrometry. Additionally, the correlation between body mass index (BMI) and the level of this amino acid in urine was accomplished. Basic parameters of urine samples were also evaluated. Statistical evaluations in the concentration of tryptophan in ASD patients with different severity of symptoms were reported. A significant difference in tryptophan levels in all groups was observed. Supplementation with B vitamins and magnesium has an influence on the Trp concentration. Furthermore, no correlation between BMI and tryptophan levels was found. These results assess that the Trp level in ASD subjects is critical and that intake of B vitamins and magnesium with diet might influence its metabolic homeostasis.
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9. Li T, Wang X, Pan J, Feng S, Gong M, Wu Y, Li G, Li S, Yi L. {{Reward learning modulates the attentional processing of faces in children with and without autism spectrum disorder}}. {Autism Res}. 2017.
The processing of social stimuli, such as human faces, is impaired in individuals with autism spectrum disorder (ASD), which could be accounted for by their lack of social motivation. The current study examined how the attentional processing of faces in children with ASD could be modulated by the learning of face-reward associations. Sixteen high-functioning children with ASD and 20 age- and ability-matched typically developing peers participated in the experiments. All children started with a reward learning task, in which the children were presented with three female faces that were attributed with positive, negative, and neutral values, and were required to remember the faces and their associated values. After this, they were tested on the recognition of the learned faces and a visual search task in which the learned faces served as the distractor. We found a modulatory effect of the face-reward associations on the visual search but not the recognition performance in both groups despite the lower efficacy among children with ASD in learning the face-reward associations. Specifically, both groups responded faster when one of the distractor faces was associated with positive or negative values than when the distractor face was neutral, suggesting an efficient attentional processing of these reward-associated faces. Our findings provide direct evidence for the perceptual-level modulatory effect of reward learning on the attentional processing of faces in individuals with ASD. Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc.
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10. McAninch DS, Heinaman AM, Lang CN, Moss KR, Bassell GJ, Rita Mihailescu M, Evans TL. {{Fragile X mental retardation protein recognizes a G quadruplex structure within the survival motor neuron domain containing 1 mRNA 5′-UTR}}. {Mol Biosyst}. 2017.
G quadruplex structures have been predicted by bioinformatics to form in the 5′- and 3′-untranslated regions (UTRs) of several thousand mature mRNAs and are believed to play a role in translation regulation. Elucidation of these roles has primarily been focused on the 3′-UTR, with limited focus on characterizing the G quadruplex structures and functions in the 5′-UTR. Investigation of the affinity and specificity of RNA binding proteins for 5′-UTR G quadruplexes and the resulting regulatory effects have also been limited. Among the mRNAs predicted to form a G quadruplex structure within the 5′-UTR is the survival motor neuron domain containing 1 (SMNDC1) mRNA, encoding a protein that is critical to the spliceosome. Additionally, this mRNA has been identified as a potential target of the fragile X mental retardation protein (FMRP), whose loss of expression leads to fragile X syndrome. FMRP is an RNA binding protein involved in translation regulation that has been shown to bind mRNA targets that form G quadruplex structures. In this study we have used biophysical methods to investigate G quadruplex formation in the 5′-UTR of SMNDC1 mRNA and analyzed its interactions with FMRP. Our results show that SMNDC1 mRNA 5′-UTR forms an intramolecular, parallel G quadruplex structure comprised of three G quartet planes, which is bound specifically by FMRP both in vitro and in mouse brain lysates. These findings suggest a model by which FMRP might regulate the translation of a subset of its mRNA targets by recognizing the G quadruplex structure present in their 5′-UTR, and affecting their accessibility by the protein synthesis machinery.
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11. McDonald NM, Murphy HG, Messinger DS. {{Empathic responding in preschool-aged children with familial risk for autism}}. {Autism Res}. 2017.
Individuals with autism spectrum disorder (ASD) show deficits in social and emotional reciprocity, which often include empathic responding. The younger siblings of children with ASD (high-risk siblings) are at elevated risk for ASD and for subclinical deficits in social-emotional functioning. Higher levels of empathy in high-risk siblings during the second and third years of life predict fewer ASD symptoms and likelihood of diagnosis. We conducted a multi-method investigation of empathic responding to an examiner’s accident in 30 low-risk and 48 high-risk siblings with (n = 12) and without ASD outcomes (n = 36) at 4-6 years of age. Empathic responding was measured through behavioral observation and parent report. Prosocial behavior did not differ by ASD outcome. Children with ASD exhibited lower levels of personal distress than high-risk and low-risk siblings without ASD. Per parent report, high-risk siblings without ASD demonstrated higher levels of empathic responding than low-risk children, while the ASD group did not differ from children without ASD on this measure. Higher levels of observed empathic concern, but not prosocial behavior, were associated with lower Social Affect scores on the Autism Diagnostic Observation Schedule in high-risk children. Results suggest that ASD diagnosis and symptoms are associated with reduced emotional responsiveness to an adult’s distress, but not associated with deficits in prosocial behavior at preschool age. Results do not support the idea that empathic responding is negatively impacted in a broader autism phenotype. Findings extend previous research by suggesting that empathy may be a protective factor in the social-emotional development of children with familial risk for ASD. Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc.
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12. Pisansky MT, Young AE, O’Connor MB, Gottesman, II, Bagchi A, Gewirtz JC. {{Mice lacking the chromodomain helicase DNA-binding 5 chromatin remodeler display autism-like characteristics}}. {Transl Psychiatry}. 2017; 7(6): e1152.
Although autism spectrum disorders (ASDs) share a core set of nosological features, they exhibit substantial genetic heterogeneity. A parsimonious hypothesis posits that dysregulated epigenetic mechanisms represent common pathways in the etiology of ASDs. To investigate this hypothesis, we generated a novel mouse model resulting from brain-specific deletion of chromodomain helicase DNA-binding 5 (Chd5), a chromatin remodeling protein known to regulate neuronal differentiation and a member of a gene family strongly implicated in ASDs. RNA sequencing of Chd5-/- mouse forebrain tissue revealed a preponderance of changes in expression of genes important in cellular development and signaling, sociocommunicative behavior and ASDs. Pyramidal neurons cultured from Chd5-/- cortex displayed alterations in dendritic morphology. Paralleling ASD nosology, Chd5-/- mice exhibited abnormal sociocommunicative behavior and a strong preference for familiarity. Chd5-/- mice further showed deficits in responding to the distress of a conspecific, a mouse homolog of empathy. Thus, dysregulated chromatin remodeling produces a pattern of transcriptional, neuronal and behavioral effects consistent with the presentation of ASDs.
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13. Ruta L, Fama FI, Bernava GM, Leonardi E, Tartarisco G, Falzone A, Pioggia G, Chakrabarti B. {{Reduced preference for social rewards in a novel tablet based task in young children with Autism Spectrum Disorders}}. {Sci Rep}. 2017; 7(1): 3329.
Atypical responsivity to social rewards has been observed in young children with or at risk of Autism Spectrum Disorders (ASD). These observations contributed to the hypothesis of reduced social motivation in ASD. In the current study we develop a novel task to test social reward preference using a tablet computer (iPad), where two differently coloured buttons were associated with a social and a nonsocial rewarding image respectively. 63 young children, aged 14-68 months, with and without a diagnosis of ASD took part in the study. The experimental sessions were also recorded on video, using an in-built webcam on the tablet as well as an external camera. Children with ASD were found to show a reduced relative preference for social rewards, indexed by a lower proportion of touches for the button associated with the social reward image. Greater social preference as measured using the tablet-based task was associated with increased use of social communicative behaviour such as eye contact with the experimenter and social smile in response to the social reward image. These results are consistent with earlier findings from eye-tracking studies, and provide novel empirical insights into atypical social reward responsivity in ASD.
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14. Saxbe DE, Golan O, Ostfeld-Etzion S, Hirschler-Guttenberg Y, Zagoory-Sharon O, Feldman R. {{HPA axis linkage in parent-child dyads: Effects of parent sex, autism spectrum diagnosis, and dyadic relationship behavior}}. {Dev Psychobiol}. 2017.
Families of preschoolers participated in two dyadic home visits, once with mother (56 dyads) and once with father (59 dyads). Each member of the dyad provided three cortisol samples and participated in several interaction tasks that were behaviorally coded. Approximately half of the children had been diagnosed with autism spectrum disorders (ASD), whereas half were typically developing (TD). In a multilevel model, father’s cortisol level at each timepoint predicted child cortisol. Father-child linkage was stronger in dyads that showed less reciprocity, in which fathers showed less sensitivity, and in which children showed less self-regulation and more withdrawal. Cortisol levels were not significantly correlated in mother-child dyads, and there was a trend toward moderation by ASD diagnosis, such that linkage was greater in TD children. Mother-child linkage was stronger in dyads that showed less behavioral coordination and less sensitivity. HPA axis linkage may be stronger in less behaviorally attuned dyads.
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15. Sayad A, Noroozi R, Omrani MD, Taheri M, Ghafouri-Fard S. {{Retinoic acid-related orphan receptor alpha (RORA) variants are associated with autism spectrum disorder}}. {Metab Brain Dis}. 2017.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with various epidemiologic, genetic, epigenetic, and environmental factors being associated with it. The observed sex bias in ASD towards male has prompted investigators to propose sex-dependent mechanisms for ASD. Retinoic acid-related orphan receptor-alpha (RORA) is a new autism candidate gene that has been shown to be differentially regulated by male and female hormones. Previous studies have shown deregulation of its expression in the prefrontal cortex and the cerebellum of ASD patients. In the present study we aimed at identification of the possible associations between two functional polymorphisms in the RORA gene (rs11639084 and rs4774388) and the risk of ASD in 518 Iranian ASD patients and 472 age, gender, and ethnic-matched healthy controls by means of tetra primer-amplification refractory mutation system-PCR. The allele and genotype frequencies of rs11639084 were not significantly different between patients and controls. However, the allele frequencies of rs4774388 showed significant overrepresentation of T allele in patients compared with controls (P = 0.04, OR (95% CI) =1.21 (1.01-1.46)). The rs4774388-TT genotype was significantly higher in patients compared with controls and was associated with ASD risk in dominant inheritance model (P = 0.04, OR (95% CI) =0.77 (0.59-0.99)). Haplotype analysis showed significant association of two estimated blocks of rs11639084/ rs4774388 with ASD risk. Consequently, the present data provide further evidence for RORA participation in the pathogenesis of ASD.
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16. Subach RM. {{Improving food choices and nutrient adequacy in adolescents/young adults with developmental disabilities}}. {Disabil Health J}. 2017.
BACKGROUND: Persons with intellectual and developmental disabilities (DD) have higher incidences of overweight and obesity than the general population and are currently underserved in health promotion programs. Restricted diets due to sensory sensitivity and physiological difference are often followed by persons with DD resulting in nutrient inadequacies, which may contribute to overweight and obesity. Closing the gap of healthcare disparities for persons with DD must start by increasing awareness of factors causing overweight and obesity, and development of strategies and programs to reduce incidences of overweight and obesity for persons with DD. OBJECTIVE: To investigate if implementation of an appropriately planned nutrition education program resulted in changes in food choices that improve the nutrient adequacy of the diet as a method of combatting or controlling incidences of obesity and overweight in persons with DD. METHODS: Pre-study, post-intervention questionnaires were administered to assess participants’ nutritional needs, aid in program design, and evaluate program appropriateness. Parental group discussions and nutrition education lessons were conducted over a 6-week period. Three-day food logs were collected and analyzed pre-study and post-intervention using the National Cancer Institute’s ASA24-2014 software. RESULTS: Results showed reductions of intake of fat, saturated fat, sodium, and sugar, and increases in intake of fiber, Vitamins A, C, and D, but there were no statistically significant differences from pre-study to post-intervention for any nutrient at the p < 0.05 level except cholesterol. CONCLUSIONS: Qualitative data indicated program success; changes in nutrient intake were insignificant, supporting the need for further research in this area. Lien vers le texte intégral (Open Access ou abonnement)
17. van Schalkwyk GI, Marin CE, Ortiz M, Rolison M, Qayyum Z, McPartland JC, Lebowitz ER, Volkmar FR, Silverman WK. {{Social Media Use, Friendship Quality, and the Moderating Role of Anxiety in Adolescents with Autism Spectrum Disorder}}. {J Autism Dev Disord}. 2017.
Social media holds promise as a technology to facilitate social engagement, but may displace offline social activities. Adolescents with ASD are well suited to capitalize on the unique features of social media, which requires less decoding of complex social information. In this cross-sectional study, we assessed social media use, anxiety and friendship quality in 44 adolescents with ASD, and 56 clinical comparison controls. Social media use was significantly associated with high friendship quality in adolescents with ASD, which was moderated by the adolescents’ anxiety levels. No associations were founds between social media use, anxiety and friendship quality in the controls. Social media may be a way for adolescents with ASD without significant anxiety to improve the quality of their friendships.
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18. Williams ME, Wheeler BY, Linder L, Jacobs RA. {{Evolving Definitions of Autism and Impact on Eligibility for Developmental Disability Services: California Case Example}}. {Intellect Dev Disabil}. 2017; 55(3): 192-209.
When establishing eligibility for developmental disability (DD) services, definitions of specific diagnostic conditions, such as autism, impact policy. Under the Medicaid home and community-based waiver program, states have discretion in determining specific program or service eligibility criteria, the nature of supports to be provided, and the number of individuals to be served. Individuals with DD, their families, and advocates have pushed to expand eligibility and improve the quality of services and supports received. This article uses a California legal case to explore the impact on individuals seeking eligibility for DD services when states rely on evolving diagnostic criteria for autism spectrum disorder. Recommendations are made for a more equitable and consistent approach to disability eligibility determination.
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19. Yang S, Guo X, Dong X, Han Y, Gao L, Su Y, Dai W, Zhang X. {{GABAA receptor subunit gene polymorphisms predict symptom-based and developmental deficits in Chinese Han children and adolescents with autistic spectrum disorders}}. {Sci Rep}. 2017; 7(1): 3290.
GABAA receptor subunit genes GABRB3, GABRA5, and GABRG3 located on chromosome 15q11-q13 have been implicated in the etiology of autistic spectrum disorders (ASD). This study intended to investigate the possible role of single-nucleotide polymorphisms (SNPs) present in GABRB3 (rs2081648 and rs1426217), GABRA5 (rs35586628), and GABRG3 (rs208129) genes in ASD susceptibility and symptom-based and developmental phenotypes of ASD in Chinese Han children and adolescents. 99 ASD patients and 231 age- and gender- frequency-matched typical developing (TD) controls were tested by TaqMan(R) genotyping assay. Symptom-based phenotypes were evaluated by Childhood Autism Rating Scale (CARS) and Autism Behavior Checklist (ABC), and developmental phenotypes were assessed by Early Childhood Development Questionnaire (ECDQ) in ASD patients. Three haplotypes and global chi 2 test of all SNPs demonstrated significant associations between ASD and TD groups. Besides, GABRB3 rs2081648, GABRA5 rs35586628, and GABRG3 rs208129 polymorphisms were associated with symptom-based deficits in social interaction, sensorimotor and somatosensory coordination, visual response, imitation, activity level, language expression and adaptability. Developmental abnormalities in late emergences of social interaction and fine motor were detected in GABRB3 rs2081648 polymorphism. Overall results indicated that gene synergy may participate in ASD pathogenesis, and GABAA receptor gene polymorphisms can predict symptom-based and developmental deficits in ASD individuals.
