1. {{Correction: Stronger Neural Modulation by Visual Motion Intensity in Autism Spectrum Disorders}}. {PLoS One};2015;10(7):e0134769.
[This corrects the article DOI: 10.1371/journal.pone.0132531.].
Lien vers le texte intégral (Open Access ou abonnement)
2. {{Developmental Disabilities Program. Final rule}}. {Fed Regist};2015 (Jul 27);80(143):44795-44827.
This rule implements the Developmental Disabilities Assistance and Bill of Rights Act of 2000. The previous regulations were completed in 1997 before the current law was passed. The rule will align the regulations and current statute and will provide guidance to AIDD grantees.
3. Almberg M, Selander H, Falkmer M, Vaz S, Ciccarelli M, Falkmer T. {{Experiences of facilitators or barriers in driving education from learner and novice drivers with ADHD or ASD and their driving instructors}}. {Dev Neurorehabil};2015 (Jul 29):1-9.
BACKGROUND: Little is known about whether individuals with autism spectrum disorder (ASD) or attention deficit hyperactive disorder (ADHD) experience any specific facilitators or barriers to driving education. OBJECTIVE: To explore the facilitators or barriers to driving education experienced by individuals with ASD or ADHD who obtained a learner’s permit, from the perspective of the learner drivers and their driving instructors. METHODS: Data were collected from 33 participants with ASD or ADHD, and nine of their driving instructors. RESULTS: Participants with ASD required twice as many driving lessons and more on-road tests than those with ADHD. Participants with ADHD repeated the written tests more than those with ASD. Driving license theory was more challenging for individuals with ADHD, whilst individuals with ASD found translating theory into practice and adjusting to « unfamiliar » driving situations to be the greatest challenges. CONCLUSION: Obtaining a driving license was associated with stressful training experience.
Lien vers le texte intégral (Open Access ou abonnement)
4. Bavin EL, Prendergast LA, Kidd E, Baker E, Dissanayake C. {{Online processing of sentences containing noun modification in young children with high-functioning autism}}. {Int J Lang Commun Disord};2015 (Jul 27)
BACKGROUND: There is variability in the language of children with autism, even those who are high functioning. However, little is known about how they process language structures in real time, including how they handle potential ambiguity, and whether they follow referential constraints. Previous research with older autism spectrum disorder (ASD) participants has shown that these individuals can use context to access rapidly the meaning of ambiguous words. The severity of autism has also been shown to influence the speed in which children with ASD access lexical information. AIMS: To understand more about how children with ASD process language in real time (i.e., as it unfolds). The focus was the integration of information and use of referential constraints to identify a referent named in a sentence. METHODS & PROCEDURES: We used an eye-tracking task to compare performance between young, high-functioning children with autism (HFA) and children with typical development (TD). A large sample of 5-9-year-old children (mean age = 6;8 years), 48 with HFA and 56 with TD participated; all were attending mainstream schools. For each item participants were shown a display of four images that differed in two dimensions. Each sentence contained an adjective and noun that restricted the choice from four to two (the target and competitor), followed by a prepositional phrase (e.g., the blue square with dots); this added modifying information to provide a unique description of the target. We calculated looking time at the target, the competitor and the two distractors for each 200 ms time interval as children processed the sentence and looked at the display. Generalized estimating equations were used to carry out repeated-measures analyses on the proportion of looking time to target and competitor and time to fixate to target. OUTCOMES & RESULTS: Children in both groups (HFA and TD) looked at the target and competitor more than at the distractors following the adjective and noun and following the modifying information in the prepositional phrase more at the target. However, the HFA group was significantly slower in both phases and looked proportionally less at the target. Across the sample, IQ and language did not affect the results; however, age and attention had an impact. The older children showed an advantage in processing the information as did the children with higher attention scores. CONCLUSIONS & IMPLICATIONS: The HFA group took longer than the TD group to integrate the disambiguating information provided in the course of processing a sentence and integrate it with the visual information, indicating that for the ASD group incremental processing was not as advanced as for children with ASD, and they were less sensitive to referential conventions. Training for young children with ASD on the use of referential conventions and available contextual clues may be of benefit to them in understanding the language they hear.
Lien vers le texte intégral (Open Access ou abonnement)
5. Cai RY, Richdale AL. {{Educational Experiences and Needs of Higher Education Students with Autism Spectrum Disorder}}. {J Autism Dev Disord};2015 (Jul 28)
Little research directly examines the needs of post-secondary students with ASD. The experiences and support needs of 23 students with ASD enrolled in two universities and four colleges, and 15 family members were explored in 15 semi-structured focus groups. Thematic analysis identified five themes: core ASD features, co-morbid conditions, transition, disclosure, and services and support. Most students felt educationally but not socially supported; most families felt support was poor in both areas. Transition from secondary school was often unplanned, and disclosure of diagnosis usually occurred after enrolment, often following a significant problem. Many parents provided substantial student support. Thus disclosure of ASD diagnosis and meeting the individual needs of these students are important considerations as higher education enrolments increase.
Lien vers le texte intégral (Open Access ou abonnement)
6. Chakrabarti B, Persico A, Battista N, Maccarrone M. {{Endocannabinoid Signaling in Autism}}. {Neurotherapeutics};2015 (Jul 28)
Autism spectrum disorder (ASD) is a complex behavioral condition with onset during early childhood and a lifelong course in the vast majority of cases. To date, no behavioral, genetic, brain imaging, or electrophysiological test can specifically validate a clinical diagnosis of ASD. However, these medical procedures are often implemented in order to screen for syndromic forms of the disorder (i.e., autism comorbid with known medical conditions). In the last 25 years a good deal of information has been accumulated on the main components of the « endocannabinoid (eCB) system », a rather complex ensemble of lipid signals (« endocannabinoids »), their target receptors, purported transporters, and metabolic enzymes. It has been clearly documented that eCB signaling plays a key role in many human health and disease conditions of the central nervous system, thus opening the avenue to the therapeutic exploitation of eCB-oriented drugs for the treatment of psychiatric, neurodegenerative, and neuroinflammatory disorders. Here we present a modern view of the eCB system, and alterations of its main components in human patients and animal models relevant to ASD. This review will thus provide a critical perspective necessary to explore the potential exploitation of distinct elements of eCB system as targets of innovative therapeutics against ASD.
Lien vers le texte intégral (Open Access ou abonnement)
7. Dababnah S, Bulson K. {{« On the Sidelines »: Access to Autism-Related Services in the West Bank}}. {J Autism Dev Disord};2015 (Jul 29)
We examined access to autism-related services among Palestinians (N = 24) raising children with autism spectrum disorder (ASD) in the West Bank. Using qualitative methods, we identified five primary interview themes. Poor screening, diagnostic, and psychoeducational practices were prevalent, as parents reported service providers minimized parental concerns and communicated ineffectively with the caregivers regarding treatment options. Geographic barriers and financial burdens prevented many families from seeking or maintaining services. Limited service availability was a dominant barrier: parents reported limited or denied access to education, community-based services, and ASD-specific interventions. Consequently, several families noted their children did not receive any services whatsoever. Research, practices and policies to address the shortage of services for children with ASD are urgently needed in the West Bank.
Lien vers le texte intégral (Open Access ou abonnement)
8. D’Hulst C, Heulens I, Van der Aa N, Goffin K, Koole M, Porke K, Van De Velde M, Rooms L, Van Paesschen W, Van Esch H, Van Laere K, Kooy RF. {{Positron Emission Tomography (PET) Quantification of GABAA Receptors in the Brain of Fragile X Patients}}. {PLoS One};2015;10(7):e0131486.
Over the last several years, evidence has accumulated that the GABAA receptor is compromised in animal models for fragile X syndrome (FXS), a common hereditary form of intellectual disability. In mouse and fly models, agonists of the GABAA receptor were able to rescue specific consequences of the fragile X mutation. Here, we imaged and quantified GABAA receptors in vivo in brain of fragile X patients using Positron Emission Topography (PET) and [11C]flumazenil, a known high-affinity and specific ligand for the benzodiazepine site of GABAA receptors. We measured regional GABAA receptor availability in 10 fragile X patients and 10 control subjects. We found a significant reduction of on average 10% in GABAA receptor binding potential throughout the brain in fragile X patients. In the thalamus, the brain region showing the largest difference, the GABAA receptor availability was even reduced with 17%. This is one of the first reports of a PET study of human fragile X brain and directly demonstrates that the GABAA receptor availability is reduced in fragile X patients. The study reinforces previous hypotheses that the GABAA receptor is a potential target for rational pharmacological treatment of fragile X syndrome.
Lien vers le texte intégral (Open Access ou abonnement)
9. Dickerson AS, Rahbar MH, Han I, Bakian AV, Bilder DA, Harrington RA, Pettygrove S, Durkin M, Kirby RS, Wingate MS, Tian LH, Zahorodny WM, Pearson DA, Moye LA, 3rd, Baio J. {{Autism spectrum disorder prevalence and proximity to industrial facilities releasing arsenic, lead or mercury}}. {Sci Total Environ};2015 (Jul 25);536:245-251.
Prenatal and perinatal exposures to air pollutants have been shown to adversely affect birth outcomes in offspring and may contribute to prevalence of autism spectrum disorder (ASD). For this ecologic study, we evaluated the association between ASD prevalence, at the census tract level, and proximity of tract centroids to the closest industrial facilities releasing arsenic, lead or mercury during the 1990s. We used 2000 to 2008 surveillance data from five sites of the Autism and Developmental Disabilities Monitoring (ADDM) network and 2000 census data to estimate prevalence. Multi-level negative binomial regression models were used to test associations between ASD prevalence and proximity to industrial facilities in existence from 1991 to 1999 according to the US Environmental Protection Agency Toxics Release Inventory (USEPA-TRI). Data for 2489 census tracts showed that after adjustment for demographic and socio-economic area-based characteristics, ASD prevalence was higher in census tracts located in the closest 10th percentile compared of distance to those in the furthest 50th percentile (adjusted RR=1.27, 95% CI: (1.00, 1.61), P=0.049). The findings observed in this study are suggestive of the association between urban residential proximity to industrial facilities emitting air pollutants and higher ASD prevalence.
Lien vers le texte intégral (Open Access ou abonnement)
10. Doshi-Velez F, Avillach P, Palmer N, Bousvaros A, Ge Y, Fox K, Steinberg G, Spettell C, Juster I, Kohane I. {{Prevalence of Inflammatory Bowel Disease Among Patients with Autism Spectrum Disorders}}. {Inflamm Bowel Dis};2015 (Jul 25)
BACKGROUND: The objective of this study was to measure the prevalence of inflammatory bowel disease (IBD) among patients with autism spectrum disorders (ASD), which has not been well described previously. METHODS: The rates of IBD among patients with and without ASD were measured in 4 study populations with distinct modes of ascertainment: a health care benefits company, 2 pediatric tertiary care centers, and a national ASD repository. The rates of IBD (established through International Classification of Diseases, Ninth Revision, Clinical Modification [ICD-9-CM] codes) were compared with respective controls and combined using a Stouffer meta-analysis. Clinical charts were also reviewed for IBD among patients with ICD-9-CM codes for both IBD and ASD at one of the pediatric tertiary care centers. This expert-verified rate was compared with the rate in the repository study population (where IBD diagnoses were established by expert review) and in nationally reported rates for pediatric IBD. RESULTS: In all of case-control study populations, the rates of IBD-related ICD-9-CM codes for patients with ASD were significantly higher than that of their respective controls (Stouffer meta-analysis, P < 0.001). Expert-verified rates of IBD among patients with ASD were 7 of 2728 patients in one study population and 16 of 7201 in a second study population. The age-adjusted prevalence of IBD among patients with ASD was higher than their respective controls and nationally reported rates of pediatric IBD. CONCLUSIONS: Across each population with different kinds of ascertainment, there was a consistent and statistically significant increased prevalance of IBD in patients with ASD than their respective controls and nationally reported rates for pediatric IBD.
Lien vers le texte intégral (Open Access ou abonnement)
11. Karakurt MN, Suren S. {{Desmopressin Use in the Treatment of Aripiprazole-Induced Nocturnal Enuresis in a Child Diagnosed with Autistic Disorder}}. {J Child Adolesc Psychopharmacol};2015 (Jul 29)
Lien vers le texte intégral (Open Access ou abonnement)
12. Kirsten TB, Chaves-Kirsten GP, Bernardes S, Scavone C, Sarkis JE, Bernardi MM, Felicio LF. {{Lipopolysaccharide Exposure Induces Maternal Hypozincemia, and Prenatal Zinc Treatment Prevents Autistic-Like Behaviors and Disturbances in the Striatal Dopaminergic and mTOR Systems of Offspring}}. {PLoS One};2015;10(7):e0134565.
Autism is characterized by social deficits, repetitive behaviors, and cognitive inflexibility. The risk factors appear to include genetic and environmental conditions, such as prenatal infections and maternal dietary factors. Previous investigations by our group have demonstrated that prenatal exposure to lipopolysaccharide (LPS), which mimics infection by gram-negative bacteria, induces autistic-like behaviors. To understand the causes of autistic-like behaviors, we evaluated maternal serum metal concentrations, which are involved in intrauterine development and infection/inflammation. We identified reduced maternal levels of zinc, magnesium, selenium and manganese after LPS exposure. Because LPS induced maternal hypozincemia, we treated dams with zinc in an attempt to prevent or ease the impairments in the offspring. We evaluated the social and cognitive autistic-like behaviors and brain tissues of the offspring to identify the central mechanism that triggers the development of autism. Prenatal LPS exposure impaired play behaviors and T-maze spontaneous alternations, i.e., it induced autistic-like behaviors. Prenatal LPS also decreased tyrosine hydroxylase levels and increased the levels of mammalian target of rapamycin (mTOR) in the striatum. Thus, striatal dopaminergic impairments may be related to autism. Moreover, excessive signaling through the mTOR pathway has been considered a biomarker of autism, corroborating our rat model of autism. Prenatal zinc treatment prevented these autistic-like behaviors and striatal dopaminergic and mTOR disturbances in the offspring induced by LPS exposure. The present findings revealed a possible relation between maternal hypozincemia during gestation and the onset of autism. Furthermore, prenatal zinc administration appears to have a beneficial effect on the prevention of autism.
Lien vers le texte intégral (Open Access ou abonnement)
13. Nava C, Rupp J, Boissel JP, Mignot C, Rastetter A, Amiet C, Jacquette A, Dupuits C, Bouteiller D, Keren B, Ruberg M, Faudet A, Doummar D, Philippe A, Perisse D, Laurent C, Lebrun N, Guillemot V, Chelly J, Cohen D, Heron D, Brice A, Closs EI, Depienne C. {{Hypomorphic variants of cationic amino acid transporter 3 in males with autism spectrum disorders}}. {Amino Acids};2015 (Jul 28)
Cationic amino acid transporters (CATs) mediate the entry of L-type cationic amino acids (arginine, ornithine and lysine) into the cells including neurons. CAT-3, encoded by the SLC7A3 gene on chromosome X, is one of the three CATs present in the human genome, with selective expression in brain. SLC7A3 is highly intolerant to variation in humans, as attested by the low frequency of deleterious variants in available databases, but the impact on variants in this gene in humans remains undefined. In this study, we identified a missense variant in SLC7A3, encoding the CAT-3 cationic amino acid transporter, on chromosome X by exome sequencing in two brothers with autism spectrum disorder (ASD). We then sequenced the SLC7A3 coding sequence in 148 male patients with ASD and identified three additional rare missense variants in unrelated patients. Functional analyses of the mutant transporters showed that two of the four identified variants cause severe or moderate loss of CAT-3 function due to altered protein stability or abnormal trafficking to the plasma membrane. The patient with the most deleterious SLC7A3 variant had high-functioning autism and epilepsy, and also carries a de novo 16p11.2 duplication possibly contributing to his phenotype. This study shows that rare hypomorphic variants of SLC7A3 exist in male individuals and suggest that SLC7A3 variants possibly contribute to the etiology of ASD in male subjects in association with other genetic factors.
Lien vers le texte intégral (Open Access ou abonnement)
14. Wong CT, Wais J, Crawford DA. {{Prenatal exposure to common environmental factors affects brain lipids and increases risk of developing Autism Spectrum Disorders}}. {Eur J Neurosci};2015 (Jul 28)
The prevalence of Autism Spectrum Disorders (ASDs) has been on the rise over recent years. The presence of diverse subsets of candidate genes in each individual with an ASD and the vast variability of phenotypical differences suggest that the interference of an exogenous environmental component may greatly contribute to the development of ASDs. The lipid mediator prostaglandin E2 (PGE2 ) is released from phospholipids of cell membranes and is important in brain development and function; PGE2 is involved in differentiation, synaptic plasticity, and calcium regulation. Our previous review already described extrinsic factors including deficient dietary supplementation and exposure to oxidative stress, infections, and inflammation that can disrupt signalling of the PGE2 pathway and contribute to ASDs. In this review, we describe the structure and establishment of two key protective barriers for the brain during early development: the blood brain barrier and the placental barrier. We then provide the first comprehensive summary of other environmental factors-such as exposure to chemicals in air pollution, pesticides, and consumer products-that can also disturb PGE2 signalling and increase the risk for developing ASDs. We also describe how these exogenous agents are capable of crossing the protective barriers of the brain during critical developmental periods when barrier components are still being formed. This review underlines the importance of avoiding or limiting exposure to these factors during vulnerable periods in development. This article is protected by copyright. All rights reserved.
Lien vers le texte intégral (Open Access ou abonnement)
15. Xiang AH. {{Maternal Diabetes and Autism in Offspring–Reply}}. {JAMA};2015 (Jul 28);314(4):407.
Lien vers le texte intégral (Open Access ou abonnement)
16. Zitser B. {{Maternal Diabetes and Autism in Offspring}}. {JAMA};2015 (Jul 28);314(4):407.
