1. Alokam R, Singhal S, Srivathsav GS, Garigipati S, Puppala S, Sriram D, Perumal Y. {{Design of dual inhibitors of ROCK-I and NOX2 as potential leads for the treatment of neuroinflammation associated with various neurological diseases including autism spectrum disorder}}. {Mol Biosyst}. 2015; 11(2): 607-17.
Inhibition of both Rho kinase (ROCK-I) and NADPH oxidase (NOX2) to treat neuroinflammation could be very effective in the treatment of progressive neurological diseases like Alzheimer’s disease, autism spectral disorder, and fragile X syndrome. NOX2 being a multi-enzyme component is activated during host defense in phagocytes such as microglia, to catalyze the production of superoxide from oxygen, while ROCK is an important mediator of fundamental cell processes like adhesion, proliferation and migration. Phosphorylated ROCK was found to activate NOX2 assembly via Ras related C3 botulinum toxin substrate (Rac) in disease conditions. Overexpression of ROCK-I and NOX2 in innate immune cells like microglial cells contribute to progressive neuronal damage early in neurological disease development. In the present study we employed a computer-aided methodology combining pharmacophores and molecular docking to identify new chemical entities that could inhibit ROCK-I as well as NOX2 (p47 phox). Among the huge dataset of a commercial database, top 18 molecules with crucial binding interactions were selected for biological evaluation. Seven among the lead molecules exhibited inhibitory potential against ROCK-I and NOX2 with IC50s ranging from 1.588 to 856.2 nM and 0.8942 to 10.24 muM, respectively, and emerged as potential hits as dual inhibitors with adequate selectivity index (SI = CC50/GIC50) in cell-based assays. The most active compound 3 was further found to show reduction of the pro-inflammatory mediators such as TNFalpha, interleukin-6 (IL-6) and interleukin-1beta (IL-1beta) mRNA expression levels in activated (MeHg treated) human neuroblastoma (IMR32) cell lines. Hence the present work documented the utility of these dual inhibitors as prototypical leads to be useful for the treatment of neurological disorders including autism spectrum disorder and Alzheimer’s disease.
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2. Bohm SR, Berger KW, Hackert PB, Renas R, Brunette S, Parker N, Padro C, Hocking A, Hedemark M, Edwards R, Bush RL, Khudyakov Y, Nelson NP, Teshale EH. {{Hepatitis a outbreak among adults with developmental disabilities in group homes – michigan, 2013}}. {MMWR Morb Mortal Wkly Rep}. 2015; 64(6): 148-52.
Hepatitis A virus (HAV) infections among persons with developmental disabilities living in institutions were common in the past, but with improvements in care and fewer persons institutionalized, the number of HAV infections has declined in these institutions. However, residents in institutions are still vulnerable if they have not been vaccinated. On April 24, 2013, a resident of a group home (GH) for adults with disabilities in southeast Michigan (GH-A) was diagnosed with hepatitis A and died 2 days later of fulminant liver failure. Four weeks later, a second GH-A resident was diagnosed with hepatitis A. None of the GH-A residents or staff had been vaccinated against hepatitis A. Over the next 3 months, six more cases of hepatitis A were diagnosed in residents in four other Michigan GHs. Three local health departments were involved in case investigation and management, including administration of postexposure prophylaxis (PEP). Serum specimens from seven cases were found to have an identical strain of HAV genotype 1A. This report describes the outbreak investigation, the challenges of timely delivery of PEP for hepatitis A, and the need for preexposure vaccination against hepatitis A for adults living or working in GHs for the disabled.
3. Bowler DM, Gaigg SB, Gardiner JM. {{Brief Report: The Role of Task Support in the Spatial and Temporal Source Memory of Adults with Autism Spectrum Disorder}}. {J Autism Dev Disord}. 2015.
Adults with autism spectrum disorder (ASD) show intact recognition (supported procedure) but impaired recall (unsupported procedure) of incidentally-encoded context. Because this has not been demonstrated for temporal source, we compared the temporal and spatial source memory of adults with ASD and verbally matched typical adults. Because of difficulties with temporal processing in ASD, we predicted ASD adults would benefit from test support for location but not temporal occurrence of studied words. We found similar levels of recognition and source memory for both groups but there was a greater effect of support on memory for location source in the ASD group. The lack of an effect of support for temporal source may simply reflect a difficulty in operationalising temporal cues.
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4. Brian JA, Bryson SE, Zwaigenbaum L. {{Autism spectrum disorder in infancy: developmental considerations in treatment targets}}. {Curr Opin Neurol}. 2015.
PURPOSE OF REVIEW: This review explores recent literature to prioritize aspects of development to be targeted by intervention for infants and toddlers with autism spectrum disorder (ASD). RECENT FINDINGS: Recent investigation of early development in ASD, including prospective studies of infants at increased risk (i.e., those with an affected older sibling) identifies impairments in four key developmental domains that are predictive of ASD. These domains are early attentional control, emotion regulation, social orienting/approach, and communication development. Reciprocal relationships exist among these domains, both in ASD and in typical development. Thus, these domains represent key intervention targets, informing treatment models under investigation in recent clinical trials. SUMMARY: By targeting the earliest and foundational manifestations of atypical development, we can capitalize on neural plasticity and build skills that are most likely to have scaffolding effects on development. The optimal timing and procedures of intervention remain empirical questions, but as the field moves toward earlier identification of risk, we are now poised to evaluate the impact of tailored approaches before the developmental cascade that leads to ASD is fully manifested. Consideration regarding community translation of ASD-specific interventions for infants and toddlers is also needed, with a focus on feasibility, cost-effectiveness, and sustainability.
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5. Chang YC, Shih W, Kasari C. {{Friendships in preschool children with autism spectrum disorder: What holds them back, child characteristics or teacher behavior?}}. {Autism}. 2015.
Children begin to show preferences for specific playmates as early as the first 2 years of life. Children with autism spectrum disorder have difficulty making friends, even in elementary and middle school. However, very little is known about earlier friendships in children with autism such as preschool friendships. This study examined friendships in preschool children with autism and explored how joint attention contributes to these friendships in mainstream settings. A secondary aim was to determine the extent to which teachers used strategies to facilitate friendship development. The participants were 31 mainstreamed preschool children (ages 2-5 years) with autism spectrum disorder. School observations were conducted individually to capture participants’ interactions with peers and adults during free play. The results indicated that 20% of the participants had friendships at school. Children with friends were more likely than children without friends to be jointly engaged with their peers during free play, and they used higher joint attention skills. Teachers used few friendship facilitating strategies, and more often used behavioral management strategies within the classrooms. Future studies may want to examine the effects of early interventions and/or teacher training on the development of friendships in preschool children with autism spectrum disorder within the school setting.
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6. De Filippis B, Valenti D, de Bari L, De Rasmo D, Musto M, Fabbri A, Ricceri L, Fiorentini C, Laviola G, Anna Vacca R. {{Mitochondrial free radicals overproduction due to respiratory chain impairment in brain of a mouse model of Rett syndrome. Protective effect of CNF1}}. {Free Radic Biol Med}. 2015.
Rett syndrome (RTT) is a pervasive neurodevelopmental disorder mainly caused by mutations in the X-linked MECP2 gene, associated with severe intellectual disability, movement disorders and autistic-like behaviours. Its pathogenesis remains mostly not understood, and no effective therapy is available. High circulating levels of oxidative stress markers in patients and the occurrence of oxidative brain damage in MeCP2-deficient mouse models suggest the involvement of oxidative stress in RTT pathogenesis. However, the molecular mechanism and the origin of oxidative stress have not been elucidated. Here we demonstrate that a redox imbalance arises from aberrant mitochondrial functionality in the brain of MeCP2-308 heterozygous female mice, the condition that more closely recapitulates that of RTT patients. The marked increase in the rate of hydrogen peroxide generation in the brain of RTT mice appears mainly produced by the dysfunctional complex II of the mitochondrial respiratory chain. In addition, both membrane potential generation and mitochondrial ATP synthesis are decreased in RTT mouse brains when succinate, the complex II respiratory substrate, is used as energy source. Respiratory chain impairment is brain area-specific, due to a decrease in either cAMP-dependent phosphorylation or protein levels of specific complex subunits. Further, we investigated whether the treatment of RTT mice with the bacterial protein CNF1, previously reported to ameliorate the neurobehavioural phenotype and brain bioenergetic markers in a RTT mouse model, exerts specific effects on brain mitochondrial function and consequently on hydrogen peroxide production. In RTT brains treated with CNF1, we observed the reactivation of respiratory chain complexes, the rescue of mitochondrial functionality and the prevention of brain hydrogen peroxide overproduction. Present results provide definitive evidence of mitochondrial reactive oxygen species overproduction in RTT mouse brain and highlight CNF1 efficacy in counteracting RTT-related mitochondrial defects.
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7. Dutheil F, Chambres P, Hufnagel C, Auxiette C, Chausse P, Ghozi R, Paugam G, Boudet G, Khalfa N, Naughton G, Chamoux A, Mermillod M, Bertrand PR. {{‘Do Well B.’: Design Of WELL Being monitoring systems. A study protocol for the application in autism}}. {BMJ Open}. 2015; 5(2): e007716.
INTRODUCTION: Individuals with autism spectrum disorder (ASD) have difficulties in communication and social interaction resulting from atypical perceptual and cognitive information processing, leading to an accumulation of anxiety. Extreme overloading experienced internally may not be externally visible. Identifying stressful situations at an early stage may avoid socially problematic behaviour from occurring, such as self-injurious behaviour. Activation of the autonomous nervous system (ANS) is involved in the response to anxiety, which can be measured through heart rate variability and skin conductance with the use of portable devices, non-intrusively and pain-free. Thus, developing innovative analysis of signal perception and reaction is necessary, mainly for non-communicative individuals with autism. METHODS AND ANALYSIS: The protocol will take place in real life (home and social environments). We aim to associate modifications of the ANS with external events that will be recorded in a synchronous manner through a specific design (spy glasses with video/audio recording). Four phases will be carried out on ASD participants and aged-matched controls: (1) 24-hour baseline pre-experiment (physical activity, sleep), (2) 2 h in a real life situation, (3) 30 min in a quiet environment, interrupted by a few seconds of stressful sound, (4) an interview to record feelings about events triggering anxiety. ASD and control participants will be together for phases 2 and 3, revealing different physiological responses to the same situations, and thus identifying potentially problematic events. The novelty will be to apply time-series analyses (which led to several Nobel Prizes in quantitative finance) on ANS series (heart rate, heart rate variability, skin conductance) and wrist motion. ETHICS AND DISSEMINATION: Ethical approval has been obtained from Ethics Committee of Clermont-Ferrand (South-East I), France (2014-A00611-46). Trial findings will be disseminated via open-access peer-reviewed publications, conferences, clinical networks, public lectures and our websites. TRIAL REGISTRATION NUMBER: ClinicalTrials identifier NCT02275455.
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8. Ebrahimi-Fakhari D, Sahin M. {{Autism and the synapse: emerging mechanisms and mechanism-based therapies}}. {Curr Opin Neurol}. 2015.
PURPOSE OF REVIEW: Recent studies have implicated hundreds of genetic variants in the cause of autism spectrum disorder (ASD). Genes involved in ‘monogenic’ forms of syndromic ASD converge on common pathways that are involved in synaptic development, plasticity and signaling. In this review, we discuss how these ‘developmental synaptopathies’ inform our understanding of the molecular disease in ASD and highlight promising approaches that have bridged the gap between the bench and the clinic. RECENT FINDINGS: Accumulating evidence suggests that synaptic deficits in syndromic and nonsyndromic ASD can be mapped to gene mutations in pathways that control synaptic protein synthesis and degradation with postsynaptic scaffold architecture and neurotransmitter receptors. This is recapitulated in models of Fragile X syndrome (FXS), Tuberous Sclerosis Complex (TSC), Angelman syndrome and Phelan-McDermid syndrome (PMS), all of which cause syndromic ASD. Important recent advances include the development of mouse models and patient-derived induced pluripotent stem cell (iPSC) lines that enable a detailed investigation of synaptic deficits and the identification of potential targets for therapy. Examples of the latter include mGluR5 antagonists in FXS, mTOR inhibitors in TSC and insulin-like growth factor 1 (IGF-1) in PMS. SUMMARY: Identifying converging pathways in syndromic forms of ASD will uncover novel therapeutic targets for non-syndromic ASD. Insights into developmental synaptopathies will lead to rational development of mechanism-based therapies and clinical trials that may provide a blueprint for other common pathways implicated in the molecular neuropathology of ASD.
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9. Fukai R, Hiraki Y, Yofune H, Tsurusaki Y, Nakashima M, Saitsu H, Tanaka F, Miyake N, Matsumoto N. {{A case of autism spectrum disorder arising from a de novo missense mutation in POGZ}}. {J Hum Genet}. 2015.
Autism spectrum disorder (ASD) is a clinically heterogeneous psychiatric disorder with various genetic backgrounds. Here, we report a novel mutation in the pogo transposable element-derived protein with zinc finger domain gene (POGZ) identified by trio-based whole exome sequencing. To date, a total of seven de novo POGZ mutations in ASD have been reported. POGZ contains a total of five functional domains, and this study reports the first de novo missense mutation in the centromere protein B-like DNA-binding domain. POGZ is highly expressed in the human fetal brain and is involved in mitosis and the regulation of neuronal proliferation. Therefore its loss-of-function or pathogenic missense mutations are likely to be causative of ASD.Journal of Human Genetics advance online publication, 19 February 2015; doi:10.1038/jhg.2015.13.
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10. Herrera JA, Ward CS, Pitcher MR, Percy AK, Skinner S, Kaufmann WE, Glaze DG, Wehrens XH, Neul JL. {{Treatment of cardiac arrhythmias in Rett Syndrome with sodium channel blocking antiepileptic drugs}}. {Dis Model Mech}. 2015.
One quarter of deaths in Rett Syndrome (RTT), an X-linked neurodevelopmental disorder, are sudden and unexpected. RTT is associated with prolonged QTc interval (LQT), and LQT-associated cardiac arrhythmias are a potential cause of unexpected death. Standard of care for LQT in RTT is treatment with beta-adrenergic antagonists; however, recent work indicates that acute treatment of mice with RTT with a beta-antagonist, propranolol, did not prevent lethal arrhythmias. In contrast, acute treatment with a sodium channel blocker, phenytoin, prevented arrhythmias. Chronic dosing of propranolol may be required for efficacy; therefore, we tested the efficacy of chronic treatment with either propranolol or phenytoin on RTT mice. Phenytoin completely abolished arrhythmias, whereas propranolol showed no benefit. Surprisingly, phenytoin also normalized weight and activity, but worsened breathing patterns. To explore the role of sodium channel blockers on QT in people with RTT, we performed a retrospective analysis of QT status before and after sodium channel blocker antiepileptic therapies. Individuals with RTT and LQT significantly improved their QT interval status after being started on sodium channel blocker antiepileptic therapies. Thus, sodium channel blockers should be considered for the clinical management of LQT in individuals with RTT.
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11. Jaber M. {{Autism is (Also) a movement disorder}}. {Mov Disord}. 2015.
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12. Jameel L, Vyas K, Bellesi G, Cassell D, Channon S. {{Great Expectations: The Role of Rules in Guiding Pro-social Behaviour in Groups with High Versus Low Autistic Traits}}. {J Autism Dev Disord}. 2015.
Measuring autistic traits in the general population has proven sensitive for examining cognition. The present study extended this to pro-social behaviour, investigating the influence of expectations to help others. A novel task describing characters in need of help was administered to students scoring high versus low on the Autism-Spectrum Quotient. Scenarios had two variants, describing either a ‘clear-cut’ or ‘ambiguous’ social rule. Participants with high versus low autistic traits were less pro-social and sympathetic overall towards the characters. The groups’ ratings of characters’ expectations were comparable, but those with high autistic traits provided more rule-based rationales in the clear-cut condition. This pattern of relatively intact knowledge in the context of reduced pro-social behaviour has implications for social skill training programmes.
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13. Kasari C. {{Update on behavioral interventions for autism and developmental disabilities}}. {Curr Opin Neurol}. 2015.
PURPOSE OF REVIEW: Given the explosion in published behavioral interventions over the past several years, this review highlights the latest trends over the past year (2014) for children with complex learning and developmental needs. RECENT FINDINGS: There were virtually no rigorous intervention studies published on developmental disorders in which the cause of the disorder is well known. Nearly all studies focus on autism spectrum disorder. Trends over the past year emphasize modular interventions with design improvements including comparisons of two active treatments and larger and more diverse samples. Far more community-implemented treatments on understudied populations were conducted, including minimally verbal children, girls, very young infants, and low-resourced families. Finally, new pilot data on prevention and neural mechanisms were published. SUMMARY: An uptick in the number of rigorous tests of different interventions conducted in real-world settings with outcomes focused on core deficits bodes well for wide dissemination and implementation by nonspecialists in the community. Pilot and uncontrolled data on prevention and mechanism await further rigorous testing before conclusions can be drawn.
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14. MacMullin JA, Lunsky Y, Weiss JA. {{Plugged in: Electronics use in youth and young adults with autism spectrum disorder}}. {Autism}. 2015.
Although electronic technology currently plays an integral role for most youth, there are growing concerns of its excessive and compulsive use. This study documents patterns and impact of electronics use in individuals with autism spectrum disorder compared to typically developing peers. Participants included 172 parents of typically developing individuals and 139 parents of individuals with an autism spectrum disorder diagnosis, ranging in age from 6 to 21 years. Parents completed an online survey of demographics and the frequency, duration, and problematic patterns of electronics use in their youth and young adults. Individuals with autism spectrum disorder were reported to use certain electronics more often in the last month and on an average day, and had greater compulsive Internet and video game use than individuals without autism spectrum disorder. Across both samples, males used video games more often than females. Compared to parents of individuals without autism spectrum disorder, parents of individuals with autism spectrum disorder were significantly more likely to report that electronics use was currently having a negative impact. The implications of problematic electronics use for individuals with autism spectrum disorder are discussed.
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15. McEvilly M, Wicks S, Dalman C. {{Sick Leave and Work Participation Among Parents of Children with Autism Spectrum Disorder in the Stockholm Youth Cohort: A Register Linkage Study in Stockholm, Sweden}}. {J Autism Dev Disord}. 2015.
This population-based register study explored the association between having a child with/without autism spectrum disorder (ASD) and parental sick leave and work participation. Parents of children with ASD living in Stockholm, Sweden in 2006 were more likely to be on sick leave, not in the labor force, or earning low income when compared to parents who did not have a child with ASD and these results remained after adjusting for familial socioeconomic factors and parental psychiatric care. Sick leave among parents was associated with having a child with ASD without intellectual disability (ID) but not ASD with ID. Although Sweden has policies helping families with children with ASD this study suggests that there exist unmet needs among these parents.
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16. Newschaffer CJ. {{Regarding Mandell and Lecavalier’s editorial « Should we believe the Centers for Disease Control and Prevention’s autism spectrum disorders prevalence estimates » and subsequent exchange with Durkin et al}}. {Autism}. 2015.
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17. Okray Z, de Esch CE, Van Esch H, Devriendt K, Claeys A, Yan J, Verbeeck J, Froyen G, Willemsen R, de Vrij FM, Hassan BA. {{A novel fragile X syndrome mutation reveals a conserved role for the carboxy-terminus in FMRP localization and function}}. {EMBO Mol Med}. 2015.
Loss of function of the FMR1 gene leads to fragile X syndrome (FXS), the most common form of intellectual disability. The loss of FMR1 function is usually caused by epigenetic silencing of the FMR1 promoter leading to expansion and subsequent methylation of a CGG repeat in the 5′ untranslated region. Very few coding sequence variations have been experimentally characterized and shown to be causal to the disease. Here, we describe a novel FMR1 mutation and reveal an unexpected nuclear export function for the C-terminus of FMRP. We screened a cohort of patients with typical FXS symptoms who tested negative for CGG repeat expansion in the FMR1 locus. In one patient, we identified a guanine insertion in FMR1 exon 15. This mutation alters the open reading frame creating a short novel C-terminal sequence, followed by a stop codon. We find that this novel peptide encodes a functional nuclear localization signal (NLS) targeting the patient FMRP to the nucleolus in human cells. We also reveal an evolutionarily conserved nuclear export function associated with the endogenous C-terminus of FMRP. In vivo analyses in Drosophila demonstrate that a patient-mimetic mutation alters the localization and function of Dfmrp in neurons, leading to neomorphic neuronal phenotypes.
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18. Rice LM, Wall CA, Fogel A, Shic F. {{Computer-Assisted Face Processing Instruction Improves Emotion Recognition, Mentalizing, and Social Skills in Students with ASD}}. {J Autism Dev Disord}. 2015.
This study examined the extent to which a computer-based social skills intervention called FaceSay was associated with improvements in affect recognition, mentalizing, and social skills of school-aged children with Autism Spectrum Disorder (ASD). FaceSay offers students simulated practice with eye gaze, joint attention, and facial recognition skills. This randomized control trial included school-aged children meeting educational criteria for autism (N = 31). Results demonstrated that participants who received the intervention improved their affect recognition and mentalizing skills, as well as their social skills. These findings suggest that, by targeting face-processing skills, computer-based interventions may produce changes in broader cognitive and social-skills domains in a cost- and time-efficient manner.
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19. Van Eylen L, Boets B, Steyaert J, Wagemans J, Noens I. {{Executive functioning in autism spectrum disorders: influence of task and sample characteristics and relation to symptom severity}}. {Eur Child Adolesc Psychiatry}. 2015.
Impaired executive functioning (EF) has been proposed to underlie symptoms of autism spectrum disorders (ASD). However, insight in the EF profile of ASD individuals is hampered due to task impurity and inconsistent findings. To elucidate these inconsistencies, we investigated the influence of task and sample characteristics on EF in ASD, with an extended test battery designed to reduce task impurity. Additionally, we studied the relation between EF and ASD symptoms. EF (inhibition, cognitive flexibility, generativity, working memory and planning) was measured in open-ended versus structured assessment situations, while controlling for possible confounding EF and non-EF variables. The performance of 50 individuals with ASD was compared with that of 50 age, gender and IQ matched typically developing (TD) individuals. The effects of group (ASD versus TD), age (children versus adolescents) and gender were examined, as well as the correlation between age, IQ, ASD symptoms and EF. Individuals with ASD showed impairments in all EF domains, but deficits were more pronounced in open-ended compared to structured settings. Group differences did not depend on gender and only occasionally on participants’ age. This suggests that inconsistencies between studies largely result from differences in task characteristics and less from differences in the investigated sample features. However, age and IQ strongly correlated with EF, indicating that group differences in these factors should be controlled for when studying EF. Finally, EF correlated with both social and non-social ASD symptoms, but further research is needed to clarify the nature of this relationship.
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20. Weisman O, Agerbo E, Carter CS, Harris JC, Uldbjerg N, Henriksen TB, Thygesen M, Mortensen PB, Leckman JF, Dalsgaard S. {{Oxytocin-augmented labor and risk for autism in males}}. {Behav Brain Res}. 2015.
The use of synthetic oxytocin (OT) to induce and/or augment labor and delivery is on the rise. Maternal exposure to OT during birth may have adverse effects on the infant’s development, including increased risk for autism. Yet, studies that test this biologically plausible association and whether it is modified by sex are limited and show inconsistent findings. To this end, we conducted an epidemiological analysis, including all singleton live births in Denmark between 2000 and 2009 (N=557,040), with a follow-up through 2012. A total of 2110 children in this cohort were subsequently diagnosed with autistic disorder according to the ICD-10-DCR. Augmentation of labor with OT was modestly associated with an increased risk for autism in males (HR 1.13; 95% CI, 1.00-1.26; P=0.04), but not in females (0.99; 0.77-1.27; P=0.95). Among males exposed to OT augmentation, 560 were subsequently diagnosed with autistic disorder, and among those not exposed, 1177 met criteria for autism (incidence rate 103.2 and 81.4 per 100,000 person-years, respectively). Our findings suggest a modest association between OT-augmented labor and risk for autism in males. However, given the known benefits of using synthetic OT during labor and delivery caution is warranted when interpreting the findings. Future studies should also investigate dose-dependent effect of OT on infant’s development.
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21. Young LJ, Barrett CE. {{Neuroscience. Can oxytocin treat autism?}}. {Science}. 2015; 347(6224): 825-6.
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22. Zhou WZ, Ye AY, Sun ZK, Tian HH, Pu TZ, Wu YY, Wang DD, Zhao MZ, Lu SJ, Yang CH, Wei L. {{Statistical analysis of twenty years (1993 to 2012) of data from mainland China’s first intervention center for children with autism spectrum disorder}}. {Mol Autism}. 2014; 5: 52.
BACKGROUND: Autism spectrum disorder (ASD) is characterized by persistent deficits in social communication and interaction, and restrictive and repetitive patterns of behavior, interests or activities. This study aimed to analyze trends in ASD diagnosis and intervention in 20 years of data from the Beijing Stars and Rain Education Institute for Autism (SR), the first autism intervention center in mainland China, and from a recent survey of members of the Heart Alliance, an industry association of autism intervention centers in China. METHODS: We analyzed the registration data at the SR from 1993 to 2012 for a total of 2,222 children who had a parent-reported diagnosis of ASD and 612 of ‘autistic tendencies’. Most of the children who were the primary focus of our analyses were age six and under. We also analyzed results of a survey we conducted in 2013 of 100 member centers of the Heart Alliance. Generalized Estimating Equations, multiple linear regression and the Mann-Whitney test were used for data analysis. Statistically significant findings are reported here. RESULTS: The number of hospitals where SR children received their diagnosis increased from several in the early 1990s to 276 at present. The proportion of ‘autistic tendencies’ diagnosis increased 2.04-fold from 1998 to 2012 and was higher for children diagnosed at a younger age. The mean age at first diagnosis of ASD or ‘autistic tendencies’ decreased by 0.27 years every decade. A higher level of parental education was statistically significantly associated with an earlier diagnosis of the child. The mean parental age at childbirth increased by about 1.48 years per decade, and the mean maternal age was 1.40 and 2.10 years higher than that in the national population censuses of 2000 and 2010, respectively. At the time of the survey 3,957 children with ASD were being trained at the 100 autism intervention centers. Ninety-seven of these centers opened after the year 2000. Economically underdeveloped regions are still underserved. CONCLUSIONS: This study revealed encouraging trends and remaining challenges in ASD diagnosis and intervention among children at the SR over the past 20 years and the 100 autism intervention centers in China at present.
