1. {{International Society For Autism Research News}}. {Autism Res}. 2015; 8(6): 801.
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2. Bitsika V, Sharpley CF, Andronicos NM, Agnew LL. {{Prevalence, structure and correlates of anxiety-depression in boys with an autism spectrum disorder}}. {Res Dev Disabil}. 2016; 49-50: 302-11.
BACKGROUND: Comorbidity of anxiety and depression predicts impaired treatment outcomes, poor quality of life and increased suicide risk. No study has reported on a combined measure of anxiety-depression in boys with an Autism Spectrum Disorder. AIMS: To explore the prevalence, underlying factor structure and relationships between anxiety-depression, physiological stress and symptoms of Autism Spectrum Disorder (ASD). METHODS: 150 boys (aged 6-18 years; IQ M=94.9, range=73-132) with an ASD plus their parents (135 mothers, 15 fathers) completed scales about the boys’ anxiety and depression, and the boys provided samples of their saliva in the morning and afternoon. Parents also completed the ASD Behaviour Checklist about the boys’ ASD symptoms. RESULTS: The two sources of ratings were not significantly different for prevalence of anxiety-depression but the factor structures varied between the parents’ and boys’ responses, with a four-factor solution for the boys’ ratings and a three-factor solution for the parents’ ratings. There were also differences in the correlations between cortisol and anxiety-depression and between ASD symptoms and anxiety depression across the boys’ and parents’ data. CONCLUSIONS: Assessment of anxiety and depression comorbidity from parents and from children with an ASD themselves could provide a valuable adjunct datum when diagnosing ASD.
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3. Esparham AE, Smith T, Belmont JM, Haden M, Wagner LE, Evans RG, Drisko JA. {{Nutritional and Metabolic Biomarkers in Autism Spectrum Disorders: An Exploratory Study}}. {Integr Med (Encinitas)}. 2015; 14(2): 40-53.
CONTEXT: Autism spectrum disorder (ASD) is currently on the rise, now affecting approximately 1 in 68 children in the United States according to a 2010 surveillance summary from the Centers for Disease Control and Prevention (CDC). This figure is an estimated increase of 78% from the figure in 2002. The CDC suggests that more investigation is needed to understand this astounding increase in autism in such a short period. OBJECTIVE: The aim of this pilot study was to determine whether a group of children with ASD exhibited similar variations in a broad array of potential correlates, including medical histories, symptoms, genetics, and multiple nutritional and metabolic biomarkers. DESIGN: This study was a retrospective, descriptive chart review. SETTING: The study took place at the University of Kansas Medical Center (KUMC). PARTICIPANTS: Participants were 7 children with ASD who had sought treatment at the Integrative Medicine Clinic at the medical center. RESULTS: A majority of the children exhibited an elevated copper:zinc ratio and abnormal vitamin D levels. Children also demonstrated abnormal levels of the essential fatty acids: (1) alpha-linolenic acid (ALA)- C13:3W3, and (2) linoleic acid (LA)-C18:2W6; high levels of docosahexaenoic acid (DHA); and an elevated omega-6:omega-3 ratio. Three of 7 children demonstrated abnormal manganese levels. Children did not demonstrate elevated urine pyruvate or lactate but did have abnormal detoxification markers. Three of 7 patients demonstrated abnormalities in citric acid metabolites, bacterial metabolism, and fatty acid oxidation markers. A majority demonstrated elevated serum immunoglobulin G (IgG) antibodies to casein, egg whites, egg yolks, and peanuts. A majority had absent glutathione S-transferase (GSTM) at the 1p13.3 location, and 3 of 7 children were heterozygous for the glutathione S-transferase I105V (GSTP1). A majority also exhibited genetic polymorphism of the mitochondrial gene superoxide dismutase A16V (SOD2). CONCLUSIONS: The findings from this small group of children with ASD points to the existence of nutritional, metabolic, and genetic correlates of ASD. These factors appear to be important potential abnormalities that warrant a case control study to evaluate their reliability and validity as markers of ASD.
4. Gardner MR, Suplee PD, Jerome-D’Emilia B. {{Survey of Nursing Faculty Preparation for Teaching About Autism Spectrum Disorders}}. {Nurse Educ}. 2016.
The prevalence of autism spectrum disorders (ASDs) has increased significantly in children and adults. Nursing faculty’s ability to teach students about best practices in their care across the lifespan is important. This study explored nurse educators’ perceived knowledge of, and levels of comfort in, their abilities to teach nursing students about nursing care of people with ASD. Strategies are proposed to incorporate competencies for care of people with ASD into nursing curricula.
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5. Lee M, Won J, Lee S, Hong Y, Kim JH. {{Benefits of Physical Exercise for Individuals with Fragile X Syndrome in Humans}}. {J Lifestyle Med}. 2015; 5(2): 35-8.
Fragile X syndrome (FXS) is the most common known genetic cause of autism spectrum disorder, and is also linked to other neurologic and psychiatric disorders. The purpose of this review article is to examine a variety of recent studies on the correlation between physical exercise and autistic behavior in individuals with fragile X syndrome. Additionally, we discuss promising approaches for further investigation of the benefits of physical exercise for autism spectrum disorder (ASD) patients. A systematic search of the PubMed digital library database for pertinent articles published from 1995 to 2011 was conducted. Individuals with ASD who experience exercise tend to exhibit improvement in physical function. In addition, exercise promotes neurotrophic factors and boosts the growth of new brain cells. The collected review articles describe how physical exercise has particular effects on stereotypic behavior and cognition among ASD patients. Finally, physical exercise may benefit patients with autism spectrum disorder through the improvement of muscular strength for increased physical capability.
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6. Levenson D. {{Dual testing strategy in autism increases diagnostic yield: Chromosomal microarray and whole-exome sequencing combination may be best for children with multiple physical anomalies, study suggests}}. {Am J Med Genet A}. 2016; 170(1): 7-8.
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7. Minshawi NF, Wink LK, Shaffer R, Plawecki MH, Posey DJ, Liu H, Hurwitz S, McDougle CJ, Swiezy NB, Erickson CA. {{A randomized, placebo-controlled trial of d-cycloserine for the enhancement of social skills training in autism spectrum disorders}}. {Mol Autism}. 2016; 7: 2.
BACKGROUND: Researchers have demonstrated that d-cycloserine (DCS) can enhance the effects of behavioral interventions in adults with anxiety and enhances prosocial behavior in animal models of autism spectrum disorders (ASD). This study extended upon this background by combining DCS with behavioral social skills therapy in youth with ASD to assess its impact on the core social deficits of ASD. We hypothesized that DCS used in combination with social skills training would enhance the acquisition of social skills in children with ASD. METHODS: A 10-week, double-blind, placebo-controlled trial of DCS (50 mg) given 30 min prior to weekly group social skills training was conducted at two sites. Children with ASD were randomized to receive 10 weeks (10 doses) of DCS or placebo in a 1:1 ratio. RESULTS: No statistically significant difference attributable to drug treatment was observed in the change scores for the primary outcome measure, the Social Responsiveness Scale (SRS), total score (p = 0.45), or on secondary outcome measures. CONCLUSIONS: The results of this trial demonstrated no drug-related short-term improvement on the primary outcome measure, or any of the secondary outcome measures. However, an overall significant improvement in SRS total raw score was observed from baseline to end of treatment for the entire group of children with ASD. This suggests a need to further study the efficacy of the social skills training protocol. Limitations to the current study and areas for future research are discussed. TRIAL REGISTRATION: ClinicalTrials.govNCT01086475.
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8. Poopal AC, Schroeder LM, Horn PS, Bassell GJ, Gross C. {{Increased expression of the PI3K catalytic subunit p110delta underlies elevated S6 phosphorylation and protein synthesis in an individual with autism from a multiplex family}}. {Mol Autism}. 2016; 7: 3.
BACKGROUND: Dysfunctions in the PI3K/mTOR pathway have gained a lot of attention in autism research. This was initially based on the discovery of several monogenic autism spectrum disorders with mutations or defects in PI3K/mTOR signaling components. Recent genetic studies corroborate that defective PI3K/mTOR signaling might be a shared pathomechanism in autism disorders of so far unknown etiology, but functional molecular analyses in human cells are rare. The goals of this study were to perform a functional screen of cell lines from patients with idiopathic autism for defects in PI3K/mTOR signaling, to test if further functional analyses are suitable to detect underlying molecular mechanisms, and to evaluate this approach as a biomarker tool to identify therapeutic targets. METHODS: We performed phospho-S6- and S6-specific ELISA experiments on 21 lymphoblastoid cell lines from the AGRE collection and on 37 lymphoblastoid cell lines from the Simons Simplex Collection and their healthy siblings. Cell lines from one individual with increased S6 phosphorylation and his multiplex family were analyzed in further detail to identify upstream defects in PI3K signaling associated with autism diagnosis. RESULTS: We detected significantly increased S6 phosphorylation in 3 of the 21 lymphoblastoid cell lines from AGRE compared to a healthy control and in 1 of the 37 lymphoblastoid cell lines from the Simons Simplex Collection compared to the healthy sibling. Further analysis of cells from one individual with elevated S6 phosphorylation showed increased expression of the PI3K catalytic subunit p110delta, which was also observed in lymphoblastoid cells from other autistic siblings but not unaffected members in his multiplex family. The p110delta-selective inhibitor IC87114 reduced elevated S6 phosphorylation and protein synthesis in this cell line. CONCLUSIONS: Our results suggest that functional analysis of PI3K/mTOR signaling is a biomarker tool to identify disease-associated molecular defects that could serve as therapeutic targets in autism. Using this approach, we discovered impaired signaling and protein synthesis through the PI3K catalytic subunit p110delta as an underlying molecular defect and potential treatment target in select autism spectrum disorders. Increased p110delta activity was recently associated with schizophrenia, and our results suggest that p110delta may also be implicated in autism.
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9. Pusponegoro HD, Ismael S, Sastroasmoro S, Firmansyah A, Vandenplas Y. {{Maladaptive Behavior and Gastrointestinal Disorders in Children with Autism Spectrum Disorder}}. {Pediatr Gastroenterol Hepatol Nutr}. 2015; 18(4): 230-7.
PURPOSE: Various gastrointestinal factors may contribute to maladaptive behavior in children with autism spectrum disorders (ASD). To determine the association between maladaptive behavior in children with ASD and gastrointestinal symptoms such as severity, intestinal microbiota, inflammation, enterocyte damage, permeability and absorption of opioid peptides. METHODS: This observational cross-sectional study compared children with ASD to healthy controls, aged 2-10 years. Maladaptive behavior was classified using the Approach Withdrawal Problems Composite subtest of the Pervasive Developmental Disorder Behavior Inventory. Dependent variables were gastrointestinal symptom severity index, fecal calprotectin, urinary D-lactate, urinary lactulose/mannitol excretion, urinary intestinal fatty acids binding protein (I-FABP) and urinary opioid peptide excretion. RESULTS: We did not find a significant difference between children with ASD with severe or mild maladaptive behavior and control subjects for gastrointestinal symptoms, fecal calprotectin, urinary D-lactate, and lactulose/mannitol ratio. Urinary opioid peptide excretion was absent in all children. Children with ASD with severe maladaptive behavior showed significantly higher urinary I-FABP levels compared to those with mild maladaptive behavior (p=0.019) and controls (p=0.015). CONCLUSION: In our series, maladaptive behavior in ASD children was not associated with gastrointestinal symptoms, intestinal inflammation (no difference in calprotectin), microbiota (no difference in urinary D-lactate) and intestinal permeability (no difference in lactulose/manitol ratio). ASD children with severe maladaptive behavior have significantly more enterocyte damage (increased urinary I-FABP) than ASD children with mild maladaptive behavior and normal children.
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10. Skonieczna-Zydecka K, Gorzkowska I, Pierzak-Sominka J, Adler G. {{The Prevalence of Autism Spectrum Disorders in West Pomeranian and Pomeranian Regions of Poland}}. {J Appl Res Intellect Disabil}. 2016.
BACKGROUND: The prevalence of autism spectrum disorders (ASD) varies worldwide from 1.4/10 000 children in the Arabian Peninsula to 185/10 000 children of Asian population. In Europe, the highest prevalence has been observed in Sweden, while the lowest in Croatia (115/10 000 and 2-3/10 000, respectively). There have been no epidemiological studies on the prevalence of ASD in Polish population. The aim of our study was to assess the prevalence of ASD in children aged 0-16 years, inhabitants of West Pomeranian and Pomeranian regions. MATERIAL AND METHODS: In total, 2514 children (2038 males, 81.1%) were included. The estimates were based on the government registries, whereas data were obtained from Provincial Disability Services Commissions. RESULTS: The prevalence of ASD in children aged 0-16 years varies between two regions of Poland – 32/10 000 in West Pomeranian and 38/10 000 in Pomeranian region. CONCLUSIONS: The average prevalence of ASD was 35/10 000 children and was about 4-fold higher in males (P < 0.05). More studies are necessary. Lien vers le texte intégral (Open Access ou abonnement)
11. Yalcin O, Kaymak G, Erdogan A, Tanidir C, Karacetin G, Kilicoglu AG, Mutlu C, Adaletli H, Gunes H, Bahali K, Ayik B, Uneri OS. {{A Retrospective Investigation of Clozapine Treatment in Autistic and Nonautistic Children and Adolescents in an Inpatient Clinic in Turkey}}. {J Child Adolesc Psychopharmacol}. 2016.
OBJECTIVE: The aim of this retrospective study is to examine the clinical outcomes and safety of clozapine in children and adolescents with schizophrenia or other psychotic disorders/autism spectrum disorder (ASD) or affective disorders. METHODS: The inpatient and outpatient files of all children and adolescents treated with clozapine over a period of 34 months (from October 2011 to July 2014) were reviewed. Demographic and clinical data were examined to describe clinical and metabolic findings, dosing, and tolerability of clozapine treatment in youth with schizophrenia, other psychotic disorders, ASD, or bipolar disorder. RESULTS: The 37 pediatric patients included 26 patients with schizophrenia or other psychotic disorders, 7 patients with ASD complicated by schizophrenia or other psychotic disorders or affective disorders, and 4 patients with ASD only. In all groups (n = 37) there was a significant reduction (p < 0.001) in Brief Psychiatric Rating Scale (BPRS) points after clozapine treatment during the inpatient period (38.78 +/- 27.75 days). In patients with schizophrenia or other psychotic disorders co-occurring with ASD or not (n = 31), there was a significant improvement in psychotic symptoms according to Positive and Negative Syndrome Scale (PANSS) total scores and subscores (p < 0.001). Of the 26 patients with schizophrenia or other psychotic disorders, 8 (30.8%) showed a positive response (>30% symptom reduction on BPRS). In patients with ASD complicated by schizophrenia or other psychotic disorders or bipolar disorders (n = 7), there was a significant reduction (p = 0.017) in BPRS scores after clozapine treatment. The discontinuation rate for clozapine was 10.8%, and the most frequently observed side effect was hypersalivation (54.1%). Neutropenia associated with clozapine was observed in only one patient (2.7%). CONCLUSIONS: Clozapine seems to be effective and safe in children and adolescents with schizophrenia or other psychotic disorders co-occuring with ASD or not. There is a need for further studies for determining the efficacy of clozapine in children and adolescents with bipolar affective disorder or ASD.
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12. Yang X, Si T, Gong Q, Qiu L, Jia Z, Zhou M, Zhao Y, Hu X, Wu M, Zhu H. {{Brain gray matter alterations and associated demographic profiles in adults with autism spectrum disorder: A meta-analysis of voxel-based morphometry studies}}. {Aust N Z J Psychiatry}. 2016.
BACKGROUND: There is increasing evidence that children with autism spectrum disorder are accompanied by specific anatomical alterations. However, the anatomical abnormalities in adults with autism spectrum disorder are poorly understood. This study was aimed to identify the neuroanatomical substrates underlying the pathophysiology of adults with autism spectrum disorder. We also investigated the relationship between neuroanatomical alterations and clinical and demographic characteristics. METHODS: A total of 13 datasets were enrolled, of which 12 studies compared whole-brain differences of 382 adult patients with autism and 393 healthy control subjects. We conducted a meta-analysis to quantitatively estimate regional gray matter volume abnormalities in individuals with autism using the effect-size signed differential mapping. RESULTS: The voxel-wise meta-analysis revealed that relative to controls, adults with autism spectrum disorder had significantly increased gray matter volume in the middle temporal gyrus, superior temporal gyrus, postcentral gyrus and parahippocampal gyrus, and reduced gray matter volume in the anterior cingulate cortex and cerebellum. Variations in gray matter volume were significantly associated with the mean age and mean total IQ score of the patients, as well as with the percentage of male patients with autism. CONCLUSION: These findings confirmed that the neuroanatomical alterations in the fronto-temporal cortices, limbic system and cerebellum in adult individuals with autism were different from the children and young adolescent’s autism. The effects of demographic characteristics on the brain morphological changes allow us to further clarify the neurobiological mechanisms and developmental trajectory in adult population with autism spectrum disorder.
