1. Anderson A, Locke J, Kretzmann M, Kasari C. {{Social network analysis of children with autism spectrum disorder: Predictors of fragmentation and connectivity in elementary school classrooms}}. {Autism};2015 (Nov 13)
Although children with autism spectrum disorder are frequently included in mainstream classrooms, it is not known how their social networks change compared to typically developing children and whether the factors predictive of this change may be unique. This study identified and compared predictors of social connectivity of children with and without autism spectrum disorder using a social network analysis. Participants included 182 children with autism spectrum disorder and 152 children without autism spectrum disorder, aged 5-12 years in 152 general education K-5 classrooms. General linear models were used to compare how age, classroom size, gender, baseline connectivity, diagnosis, and intelligence quotient predicted changes in social connectivity (closeness). Gender and classroom size had a unique interaction in predicting final social connectivity and the change in connectivity for children with autism spectrum disorder; boys who were placed in larger classrooms showed increased social network fragmentation. This increased fragmentation for boys when placed in larger classrooms was not seen in typically developing boys. These results have implications regarding placement, intervention objectives, and ongoing school support that aimed to increase the social success of children with autism spectrum disorder in public schools.
Lien vers le texte intégral (Open Access ou abonnement)
2. Bahmani M, Sarrafchi A, Shirzad H, Rafieian-Kopaei M. {{Autism: Pathophysiology and promising herbal remedies}}. {Curr Pharm Des};2015 (Nov 12)
Autism is a comprehensive growth abnormality in which social skills, language, communication, and behavioral skills are developed with delay and as diversionary. The reasons for autism are unclear, but various theories of genetics, immunity, biological, and psychosocial factors have been proffered. In fact, autism is a complex disorder with distinct causes that usually co-occur. Although no medicine has been recognized to treat this disorder, pharmacological treatments can be effective in reducing its signs, such as self-mutilation, aggression, repetitive and stereotyped behaviors, inattention, hyperactivity, and sleeping disorders. Recently, complementary and alternative approaches have been considered to treat autism. Ginkgo biloba is one of the most effective plants with an old history of applications in neuropsychological disorders which recently is used for autism. The present review discusses the recent findings, pathophysiology, and etiology of autism and thereafter addresses the promising results of herbal remedies.
3. Goldin RL, Matson JL, Matheis M, Jang J. {{The relationship between premature birth and caregiver first concern in toddlers with autism spectrum disorder: A brief report}}. {Child Neuropsychol};2015 (Nov 11):1-7.
The current study examines the relationship between premature birth and the age at which caregivers first become concerned with their child’s development in a sample of 84 toddlers with autism spectrum disorder (ASD). The participants were split into two groups: those born prematurely and those born full term. The results indicate that the age of caregiver first concern is significantly younger for those born prematurely than those born full term. The average age caregivers reported first becoming concerned about their child’s development was around 7 months for participants born prematurely and around 13 months for participants born full term. Possible explanations for the results and their implications are discussed.
Lien vers le texte intégral (Open Access ou abonnement)
4. Goldschmidt J. {{Nutritional Status and Autism Spectrum Disorders}}. {Adv Nutr};2015 (Nov);6(6):865.
Lien vers le texte intégral (Open Access ou abonnement)
5. House SA, Goodman DC, Weinstein SJ, Chang CH, Wasserman JR, Morden NE. {{Prescription Use among Children with Autism Spectrum Disorders in Northern New England: Intensity and Small Area Variation}}. {J Pediatr};2015 (Nov 7)
OBJECTIVE: To measure prescription use intensity and regional variation of psychotropic and 2 important nonpsychotropic drug groups among children with autism spectrum disorders (ASDs) compared with children in the general population. STUDY DESIGN: Cross-sectional study of ambulatory prescription fills from Maine, Vermont, and New Hampshire all-payer administrative data, 2007-2010. RESULTS: Overall there were 13 100 children diagnosed with ASD (34 584 person years [PYs]) and 936 721 (1.7 million PYs) without ASD diagnosis. The overall prescription fill rate was 16.6 per PY in children with ASD and 4.1 per PY in the general population. Psychotropic use among children with ASDs was 9-fold the general population rate (7.80 vs 0.85 fills per PY); these children comprised 2.0% of the pediatric population but received 15.6% of psychotropics. Nonpsychotropic drug use was also higher in the population with ASD, particularly the youngest: among those under age 3 years, antibiotic use was 2-fold and antacid use nearly 5-fold the general population rate (3.2 vs 1.4 and 1.0 vs 0.2 per PY, respectively). Among children with ASDs, prescription use varied substantially across hospital service areas, as much as 3-fold for antacids and alpha agonists, more than 4-fold for benzodiazepines (5th to 95th percentile). CONCLUSIONS: The overall psychotropic and nonpsychotropic prescription intensity among children with ASDs is characterized by broad regional variation, suggesting diverse provider responses to pharmacotherapeutic uncertainty. This variation highlights a need for more research, practice-based learning, and shared decision making with caregivers surrounding therapy for children with ASDs.
Lien vers le texte intégral (Open Access ou abonnement)
6. Ingersoll B, Berger N. {{Correction: Parent Engagement With a Telehealth-Based Parent-Mediated Intervention Program for Children With Autism Spectrum Disorders: Predictors of Program Use and Parent Outcomes}}. {J Med Internet Res};2015;17(11):e257.
[This corrects the article DOI: 10.2196/jmir.4913.].
Lien vers le texte intégral (Open Access ou abonnement)
7. Jaramillo TC, Speed HE, Xuan Z, Reimers JM, Liu S, Powell CM. {{Altered Striatal Synaptic Function and Abnormal Behaviour in Shank3 Exon4-9 Deletion Mouse Model of Autism}}. {Autism Res};2015 (Nov 11)
Shank3 is a multi-domain, synaptic scaffolding protein that organizes proteins in the postsynaptic density of excitatory synapses. Clinical studies suggest that approximately 0.5% of autism spectrum disorder (ASD) cases may involve SHANK3 mutation/deletion. Patients with SHANK3 mutations exhibit deficits in cognition along with delayed/impaired speech/language and repetitive and obsessive/compulsive-like (OCD-like) behaviors. To examine how mutation/deletion of SHANK3 might alter brain function leading to ASD, we have independently created mice with deletion of Shank3 exons 4-9, a region implicated in ASD patients. We find that homozygous deletion of exons 4-9 (Shank3e4-9 KO) results in loss of the two highest molecular weight isoforms of Shank3 and a significant reduction in other isoforms. Behaviorally, both Shank3e4-9 heterozygous (HET) and Shank3e4-9 KO mice display increased repetitive grooming, deficits in novel and spatial object recognition learning and memory, and abnormal ultrasonic vocalizations. Shank3e4-9 KO mice also display abnormal social interaction when paired with one another. Analysis of synaptosome fractions from striata of Shank3e4-9 KO mice reveals decreased Homer1b/c, GluA2, and GluA3 expression. Both Shank3e4-9 HET and KO demonstrated a significant reduction in NMDA/AMPA ratio at excitatory synapses onto striatal medium spiny neurons. Furthermore, Shank3e4-9 KO mice displayed reduced hippocampal LTP despite normal baseline synaptic transmission. Collectively these behavioral, biochemical and physiological changes suggest Shank3 isoforms have region-specific roles in regulation of AMPAR subunit localization and NMDAR function in the Shank3e4-9 mutant mouse model of autism. Autism Res 2015. (c) 2015 International Society for Autism Research, Wiley Periodicals, Inc.
Lien vers le texte intégral (Open Access ou abonnement)
8. Kobayashi T, Hirano Y, Nemoto K, Sutoh C, Ishikawa K, Miyata H, Matsumoto J, Matsumoto K, Masuda Y, Nakazato M, Shimizu E, Nakagawa A. {{Correlation between Morphologic Changes and Autism Spectrum Tendency in Obsessive-Compulsive Disorder}}. {Magn Reson Med Sci};2015 (Nov 13);14(4):329-335.
OBJECTIVES: Obsessive-compulsive disorder (OCD) is one of the most debilitating psychiatric disorders, with some speculating that a reason for difficulty in its treatment might be its coexistence with autism spectrum. We investigated the tendency for autistic spectrum disorders (ASD) in patients with OCD from a neuroimaging point of view using voxel-based morphometry. METHODS: We acquired T1-weighted images from 20 patients with OCD and 30 healthy controls and investigated the difference in regional volume between the groups as well as the correlation between Autism-Spectrum Quotient (AQ) scores and regional cerebral volumes of patients with OCD. RESULTS: Volumes in the bilateral middle frontal gyri were significantly decreased in patients with OCD compared to controls. Correlational analysis showed significant positive correlations between AQ scores and regional gray matter (GM) volumes in the left dorsolateral prefrontal cortex (DLPFC) and left amygdala. Furthermore, GM volumes of these regions were positively correlated with each other. CONCLUSIONS: The positive correlation of ASD traits in patients with OCD with regional GM volumes in the left DLPFC and amygdala could reflect the heterogeneity of patient symptoms. Our results suggest that differences in GM volume might allow classification of patients with OCD for appropriate therapy based on their particular traits.
Lien vers le texte intégral (Open Access ou abonnement)
9. Li J, You Y, Yue W, Jia M, Yu H, Lu T, Wu Z, Ruan Y, Wang L, Zhang D. {{Genetic Evidence for Possible Involvement of the Calcium Channel Gene CACNA1A in Autism Pathogenesis in Chinese Han Population}}. {PLoS One};2015;10(11):e0142887.
Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders. Recent studies suggested that calcium channel genes might be involved in the genetic etiology of ASD. CACNA1A, encoding an alpha-1 subunit of voltage-gated calcium channel, has been reported to play an important role in neural development. Previous study detected that a single nucleotide polymorphism (SNP) in CACNA1A confers risk to ASD in Central European population. However, the genetic relationship between autism and CACNA1A in Chinese Han population remains unclear. To explore the association of CACNA1A with autism, we performed a family-based association study. First, we carried out a family-based association test between twelve tagged SNPs and autism in 239 trios. To further confirm the association, the sample size was expanded to 553 trios by recruiting 314 additional trios. In a total of 553 trios, we identified association of rs7249246 and rs12609735 with autism though this would not survive after Bonferroni correction. Our findings suggest that CACNA1A might play a role in the etiology of autism.
Lien vers le texte intégral (Open Access ou abonnement)
10. Meier SM, Petersen L, Schendel DE, Mattheisen M, Mortensen PB, Mors O. {{Obsessive-Compulsive Disorder and Autism Spectrum Disorders: Longitudinal and Offspring Risk}}. {PLoS One};2015;10(11):e0141703.
BACKGROUND: Despite substantial similarities and overlaps in the pathophysiology of obsessive-compulsive disorders (OCD) and autism spectrum disorders, little is known about the clinical and etiologic cohesion of these two disorders. We therefore aimed to determine the patterns of comorbidity, longitudinal risks, and shared familial risks between these disorders. METHODS: In a prospective study design we explored the effect of a prior diagnosis of OCD in patients and parents on the susceptibility to autism spectrum disorders and vice versa. Analyses were adjusted for sex, age, calendar year, parental age and place at residence at time of birth. As measures of relative risk incidence rate ratios (IRR) and accompanying 95% confidence intervals (CIs) were employed. RESULTS: The risk of a comorbid diagnosis of OCD in individuals with autism spectrum disorder and aggregation of autism spectrum disorders in offspring of parents with OCD were increased. Individuals first diagnosed with autism spectrum disorders had a 2-fold higher risk of a later diagnosis of OCD (IRR = 2.18, 95% CI = 1.91-2.48), whereas individuals diagnosed with OCD displayed a nearly 4-fold higher risk to be diagnosed with autism spectrum disorders (IRR = 3.91, 95% CI = 3.46-4.40) later in life. The observed associations were somewhat stronger for less severe types of autism spectrum disorders without a comorbid diagnosis of mental disabilities. CONCLUSIONS: The high comorbidity, sequential risk, and shared familial risks between OCD and autism spectrum disorders are suggestive of partially shared etiological mechanisms. The results have implications for current gene-searching efforts and for clinical practice.
Lien vers le texte intégral (Open Access ou abonnement)
11. Mottron L. {{[Is psychiatry relevant in autism? A brief historical perspective on the role of psychiatry in diagnosis, and support to autistic people]}}. {Sante Ment Que};2015 (Summer);40(2):177-190.
Based on an overview of the recent history of professional roles in autism diagnosis and support in the province of Quebec, this paper supports the view that hearing what autistic people say, combined with interdisciplinary, but hierarchically ruled task sharing in clinical settings, and to a pacific confrontation between scientific and clinical demands, prevents the high jacking of autism for corporatist or ideological purposes.
12. Nazareth T, Li N, Marynchenko M, Zhou Z, Chopra P, Signorovitch J, Wu E, Ahmed S, Marvel J, Sasane R. {{Burden of Illness among Patients with Fragile X Syndrome (FXS): A Medicaid Perspective}}. {Curr Med Res Opin};2015 (Nov 13):1-47.
BACKGROUND: Fragile X Syndrome (FXS) is an inherited intellectual disability that imposes a substantial clinical and humanistic burden on patients and caregivers. This study aimed to quantify the incremental burden of illness following FXS diagnosis in Medicaid populations. METHODS: A retrospective matched-cohort study was conducted using FL, NJ, MO, IA, and KS Medicaid claims (1997-2012). Patients with FXS were matched 1:5 to a comparison group without FXS, based on age, gender, state, and continuous Medicaid coverage. Healthcare resource utilization and costs were compared among cohorts over 1 year following first diagnosis. RESULTS: Overall, 697 patients with FXS were matched to 3,485 non-FXS patients. Median age was 12.0 years; 82% were male. Newly diagnosed FXS patients were younger (median age: 7.0 years). During the follow-up, patients with FXS had significantly higher medication use, medical procedure use, medical specialist visits, and associated costs than the non-FXS comparison group. One-fourth of FXS patients filled prescriptions for stimulants, antipsychotics, or anticonvulsants; 25% of patients with FXS had speech and language therapy and 39% had physical therapy (versus 9%, 4% and 8%, respectively, for the comparison group). At least 44% of FXS patients visited a neurologist, cardiologist, otolaryngologist, or gastroenterologist; 92% of patients with FXS had an outpatient visit, 35% had an emergency room visit, and 34% used home services (compared to 31%-32%, 64%, 27%, and 10%, respectively, for the comparison group) (all p<0.05). Patients with FXS had an incremental annual total healthcare cost of $33,409 (2012$) per person relative to the comparison group, while newly diagnosed FXS patients had incremental total annual healthcare costs of $17,617 (2012$) per person. CONCLUSIONS: Both established and newly diagnosed FXS were associated with significantly increased use of multiple medications and medical services, and increased healthcare costs. Treatments that could help reduce this disease burden are urgently needed. Lien vers le texte intégral (Open Access ou abonnement)
13. Provenzano G, Sgado P, Genovesi S, Zunino G, Casarosa S, Bozzi Y. {{Hippocampal dysregulation of FMRP/mGluR5 signaling in engrailed-2 knockout mice: a model of autism spectrum disorders}}. {Neuroreport};2015 (Dec 16);26(18):1101-1105.
Many evidences indicate that mice lacking the homeobox transcription factor engrailed-2 (En2 mice) represent a reliable model to investigate neurodevelopmental basis and gene expression changes relevant to autism spectrum disorders. Dysfunctions in fragile X mental retardation protein (FMRP), metabotropic glutamate receptor 5 (mGluR5), and GABAergic signaling pathways have been proposed as a possible pathogenic mechanism of autism spectrum disorders. Here, we exploited En2 mice to investigate hippocampal expression of FMRP, mGluR5, and GABAA receptor beta3 subunit (GABRB3). Quantitative reverse-transcription PCR showed that all these mRNAs were significantly downregulated in En2 mice compared with wild-type littermates. Western blot and immunohistochemistry confirmed the downregulation of FMRP and GABRB3 proteins, while showing a significant increase of mGluR5 protein in the En2 hippocampus. Our results suggest that the dysregulation of FMRP-mGluR5 signaling pathway, accompanied with a downregulation of GABRB3 expression, may contribute to the ‘autistic-like’ features observed in En2 mice, providing possible molecular targets for future pharmacological studies.
Lien vers le texte intégral (Open Access ou abonnement)
14. Sellinger VJ, Elder JH. {{Parent Training Intervention to Manage Externalizing Behaviors in Children With Autism}}. {J Pediatr Health Care};2015 (Nov 7)
Children with autism spectrum disorder (ASD) are more likely than their typically developing peers to exhibit externalizing behaviors; however, the etiology in children with ASD may be different and related to the core deficits of the disorder. Although parent training interventions have been effective in decreasing externalizing behaviors in typically developing children, the effectiveness in children with ASD has not been established. An in-depth analysis of the child’s behavior may provide the foundation upon which to develop an individualized parent training approach. This case study illustrates how a functional assessment interview was used to obtain in-depth information about externalizing behaviors exhibited by a child with ASD who is high functioning and how this information was used to develop an individualized parent training intervention.
Lien vers le texte intégral (Open Access ou abonnement)
15. Wei H, Ma Y, Liu J, Ding C, Hu F, Yu L. {{Proteomic analysis of cortical brain tissue from the BTBR mouse model of autism: Evidence for changes in stop and myelin-related proteins}}. {Neuroscience};2015 (Nov 10)
Autism is a neurodevelopmental disorder characterized by abnormal reciprocal social interactions, communication deficits, and repetitive behaviors with restricted interests. However, the widely accepted biomarkers for autism are still lacking. In this study, we carried out a quantitative proteomic profiling study of cortical brain tissue from BTBR T+Itpr3tf (BTBR) mice, a mouse model that displays an autism-like phenotype. Using isobaric tag for relative and absolute quantification (iTRAQ) coupled with LC-MS/MS, a total of 3611 proteins were quantitated in mouse cortices. As compared to C57BL/6J (B6) mice, 126 differentially expressed proteins were found in the brain from BTBR mice. The functional annotation and categories of differentially expressed proteins were analyzed. Especially, the stable tubule only polypeptide (STOP) protein and myelin-related proteins down-regulated significantly in BTBR mice were confirmed by Western blotting. Furthermore, the BTBR mice displayed reduced levels of staining with ferric alum in comparison to B6 controls, indicative of myelin disruption. Finally, we propose that reduced STOP expression in the brain could be involved in the mediation of autism-like behaviors through impairments of myelination in oligodendrocytes and synaptic function in neurons. Manipulation of STOP protein could be a promising avenue for therapeutic interventions to autism.
Lien vers le texte intégral (Open Access ou abonnement)
16. Werling AM, Bobrowski E, Taurines R, Gundelfinger R, Romanos M, Grunblatt E, Walitza S. {{CNTNAP2 gene in high functioning autism: no association according to family and meta-analysis approaches}}. {J Neural Transm (Vienna)};2015 (Nov 11)
The Contactin Associated Protein-like 2 (CNTNAP2) gene has been discussed to be associated with different symptoms of autism spectrum disorders (ASDs) and other neurodevelopmental disorders. We aimed to elucidate the genetic association of CNTNAP2 within high functioning ASD (HFA), focusing on autism specific symptoms and reducing intelligence related factors. Furthermore, we compared our findings conducting a meta-analysis in patients with ASD and HFA only. A case-control association study was performed for HFA (HFA, n = 105; controls, n = 133). Moreover, we performed a family-based association study (DFAM) analysis (HFA, n = 44; siblings, n = 57). Individuals were genotyped for the two most frequently reported single nucleotide polymorphisms (SNPs) in the CNTNAP2 gene (rs2710102, rs7794745). Furthermore, a meta-analysis using the MIX2 software integrated our results with previously published data. A significant association for the carriers of the T-allele of the rs7794745 with HFA was found in the case-control sample [OR = 1.547; (95 % CI 1.056-2.266); p = 0.025]. No association could be found by DFAM with any of the CNTNAP2 SNPs with HFA. The meta-analysis of both SNPs did not show a significant association with either ASD or with HFA. Overall, including case-control, sibs, and meta-analysis, we could not detect any significant association with the CNTNAP2 gene and HFA. Our results point in the direction that CNTNAP2 may not play a major role in HFA, but rather seems to have a significance in neurodevelopmental disorders or in individuals displaying intellectual delays.
