1. Bjornsdotter M, Wang N, Pelphrey K, Kaiser MD. {{Evaluation of Quantified Social Perception Circuit Activity as a Neurobiological Marker of Autism Spectrum Disorder}}. {JAMA Psychiatry}. 2016.
Importance: Autism spectrum disorder (ASD) is marked by social disability and is associated with dysfunction in brain circuits supporting social cue perception. The degree to which neural functioning reflects individual-level behavioral phenotype is unclear, slowing the search for functional neuroimaging biomarkers of ASD. Objective: To examine whether quantified neural function in social perception circuits may serve as an individual-level marker of ASD in children and adolescents. Design, Setting, and Participants: The cohort study was conducted at the Yale Child Study Center and involved children and adolescents diagnosed as having ASD and typically developing participants. Participants included a discovery cohort and a larger replication cohort. Individual-level social perception circuit functioning was assessed as functional magnetic resonance imaging brain responses to point-light displays of coherent vs scrambled human motion. Main Outcomes and Measures: Outcome measures included performance of quantified brain responses in affected male and female participants in terms of area under the receiver operating characteristic curve (AUC), sensitivity and specificity, and correlations between brain responses and social behavior. Results: Of the 39 participants in the discovery cohort aged 4 to 17 years, 22 had ASD and 30 were boys. Of the 75 participants in the replication cohort aged 7 to 20 years, 37 had ASD and 52 were boys. A relative reduction in social perception circuit responses was identified in discovery cohort boys with ASD at an AUC of 0.75 (95% CI, 0.52-0.89; P = .01); however, typically developing girls and girls with ASD could not be distinguished (P = .54). The results were confirmed in the replication cohort, where brain responses were identified in boys with ASD at an AUC of 0.79 (95% CI, 0.64-0.91; P < .001) and failed to distinguish affected and unaffected girls (P = .82). Across both cohorts, boys were identified at an AUC of 0.77 (95% CI, 0.64-0.86) with corresponding sensitivity and specificity of 76% each. Additionally, brain responses were associated with social behavior in boys but not in girls. Conclusions and Relevance: Quantified social perception circuit activity is a promising individual-level candidate neural marker of the male ASD behavioral phenotype. Our findings highlight the need to better understand effects of sex on social perception processing in relation to ASD phenotype manifestations. Lien vers le texte intégral (Open Access ou abonnement)
2. Bone D, Bishop S, Black MP, Goodwin MS, Lord C, Narayanan SS. {{Use of machine learning to improve autism screening and diagnostic instruments: effectiveness, efficiency, and multi-instrument fusion}}. {J Child Psychol Psychiatry}. 2016.
BACKGROUND: Machine learning (ML) provides novel opportunities for human behavior research and clinical translation, yet its application can have noted pitfalls (Bone et al., 2015). In this work, we fastidiously utilize ML to derive autism spectrum disorder (ASD) instrument algorithms in an attempt to improve upon widely used ASD screening and diagnostic tools. METHODS: The data consisted of Autism Diagnostic Interview-Revised (ADI-R) and Social Responsiveness Scale (SRS) scores for 1,264 verbal individuals with ASD and 462 verbal individuals with non-ASD developmental or psychiatric disorders, split at age 10. Algorithms were created via a robust ML classifier, support vector machine, while targeting best-estimate clinical diagnosis of ASD versus non-ASD. Parameter settings were tuned in multiple levels of cross-validation. RESULTS: The created algorithms were more effective (higher performing) than the current algorithms, were tunable (sensitivity and specificity can be differentially weighted), and were more efficient (achieving near-peak performance with five or fewer codes). Results from ML-based fusion of ADI-R and SRS are reported. We present a screener algorithm for below (above) age 10 that reached 89.2% (86.7%) sensitivity and 59.0% (53.4%) specificity with only five behavioral codes. CONCLUSIONS: ML is useful for creating robust, customizable instrument algorithms. In a unique dataset comprised of controls with other difficulties, our findings highlight the limitations of current caregiver-report instruments and indicate possible avenues for improving ASD screening and diagnostic tools.
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3. Cantio C, Jepsen JR, Madsen GF, Bilenberg N, White SJ. {{Exploring ‘The autisms’ at a cognitive level}}. {Autism Res}. 2016.
The autism spectrum is characterized by genetic and behavioral heterogeneity. However, it is still unknown whether there is a universal pattern of cognitive impairment in autism spectrum disorder (ASD) and whether multiple cognitive impairments are needed to explain the full range of behavioral symptoms. This study aimed to determine whether three widely acknowledged cognitive abnormalities (Theory of Mind (ToM) impairment, Executive Function (EF) impairment, and the presence of a Local Processing Bias (LB)) are universal and fractionable in autism, and whether the relationship between cognition and behavior is dependent on the method of behavioral assessment. Thirty-one high-functioning children with ASD and thirty-seven children with neurotypical development (NTD), comparable in age, gender and Intelligence Quotient (IQ), completed several tasks tapping into ToM, EF, and LB, and autistic symptomatology was assessed through parental and teacher questionnaires, parental interview and direct observation. We found that ToM and EF deficits differentiated the groups and some ToM and EF tasks were related to each other. ToM and EF were together able to correctly classify more than three-quarters of the children into cases and controls, despite relating to none of the specific behavioral measures. Only a small subgroup of individuals displayed a LB, which was unrelated to ToM and EF, and did not aid diagnostic classification, most likely contributing to non-diagnostic symptoms in a subgroup. Despite the characteristic heterogeneity of the autism spectrum, it remains a possibility therefore that a single cognitive cause may underlie the range of diagnostic symptoms in all individuals with autism. Autism Res 2016,. (c) 2016 International Society for Autism Research, Wiley Periodicals, Inc.
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4. Cascio CJ, Woynaroski T, Baranek GT, Wallace MT. {{Toward an interdisciplinary approach to understanding sensory function in autism spectrum disorder}}. {Autism Res}. 2016.
Heightened interest in sensory function in persons with autism spectrum disorder (ASD) presents an unprecedented opportunity for impactful, interdisciplinary work between neuroscientists and clinical practitioners for whom sensory processing is a focus. In spite of this promise, and a number of overlapping perspectives on sensory function in persons with ASD, neuroscientists and clinical practitioners are faced with significant practical barriers to transcending disciplinary silos. These barriers include divergent goals, values, and approaches that shape each discipline, as well as different lexical conventions. This commentary is itself an interdisciplinary effort to describe the shared perspectives, and to conceptualize a framework that may guide future investigation in this area. We summarize progress to date and issue a call for clinical practitioners and neuroscientists to expand cross-disciplinary dialogue and to capitalize on the complementary strengths of each field to unveil the links between neural and behavioral manifestations of sensory differences in persons with ASD. Joining forces to face these challenges in a truly interdisciplinary way will lead to more clinically informed neuroscientific investigation of sensory function, and better translation of those findings to clinical practice. Likewise, a more coordinated effort may shed light not only on how current approaches to treating sensory processing differences affect brain and behavioral responses to sensory stimuli in individuals with ASD, but also on whether such approaches translate to gains in broader characteristics associated with ASD. It is our hope that such interdisciplinary undertakings will ultimately converge to improve assessment and interventions for persons with ASD. Autism Res 2016,. (c) 2016 International Society for Autism Research, Wiley Periodicals, Inc.
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5. Ethridge LE, White SP, Mosconi MW, Wang J, Byerly MJ, Sweeney JA. {{Reduced habituation of auditory evoked potentials indicate cortical hyper-excitability in Fragile X Syndrome}}. {Transl Psychiatry}. 2016; 6: e787.
Sensory hypersensitivities are common, clinically distressing features of Fragile X Syndrome (FXS). Preclinical evidence suggests this abnormality may result from synaptic hyper-excitability in sensory systems. This model predicts reduced sensory habituation to repeated stimulus presentation. Fourteen adolescents and adults with FXS and 15 age-matched controls participated in a modified auditory gating task using trains of 4 identical tones during dense array electroencephalography (EEG). Event-related potential and single trial time-frequency analyses revealed decreased habituation of the N1 event-related potential response in FXS, and increased gamma power coupled with decreases in gamma phase-locking during the early-stimulus registration period. EEG abnormalities in FXS were associated with parent reports of heightened sensory sensitivities and social communication deficits. Reduced habituation and altered gamma power and phase-locking to auditory cues demonstrated here in FXS patients parallels preclinical findings with Fmr1 KO mice. Thus, the EEG abnormalities seen in FXS patients support the model of neocortical hyper-excitability in FXS, and may provide useful translational biomarkers for evaluating novel treatment strategies targeting its neural substrate.
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6. Hecht PM, Hudson M, Connors SL, Tilley MR, Liu X, Beversdorf DQ. {{Maternal serotonin transporter genotype affects risk for ASD with exposure to prenatal stress}}. {Autism Res}. 2016.
Stress exposure during gestation is implicated in several neuropsychiatric conditions, including autism spectrum disorder (ASD). Previous research showed that prenatal stress increases risk for ASD with peak exposure during the end of the second and the beginning of the third trimester. However, exposures to prenatal stress do not always result in ASD, suggesting that other factors may interact with environmental stressors to increase ASD risk. The present study examined a maternal genetic variation in the promoter region of the serotonin transporter gene (5-HTTLPR) affecting stress tolerance and its interaction with the effect of environmental stressors on risk for ASD. Two independent cohorts of mothers of ASD children recruited by the University of Missouri and Queen’s University were surveyed regarding the prenatal environment and genotyping on 5-HTTLPR was performed to explore this relationship. In both samples, mothers of children with ASD carrying the stress susceptible short allele variant of 5-HTTLPR experienced a greater number of stressors and greater stress severity when compared to mothers carrying the long allele variant. The temporal peak of stressors during gestation in these mothers was consistent with previous findings. Additionally, increased exposure to prenatal stress was not reported in the pregnancies of typically developing siblings from the same mothers, regardless of maternal genotype, suggesting against the possibility that the short allele might increase the recall of stress during pregnancy. The present study provides further evidence of a specific maternal polymorphism that may affect the risk for ASD with exposure to prenatal stress. Autism Res 2016. (c) 2016 International Society for Autism Research, Wiley Periodicals, Inc.
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7. Kirby AV, Boyd BA, Williams KL, Faldowski RA, Baranek GT. {{Sensory and repetitive behaviors among children with autism spectrum disorder at home}}. {Autism}. 2016.
Atypical sensory and repetitive behaviors are defining features of autism spectrum disorder and are thought to be influenced by environmental factors; however, there is a lack of naturalistic research exploring contexts surrounding these behaviors. This study involved video recording observations of 32 children with autism spectrum disorder (2-12 years of age) engaging in sensory and repetitive behaviors during home activities. Behavioral coding was used to determine what activity contexts, sensory modalities, and stimulus characteristics were associated with specific behavior types: hyperresponsive, hyporesponsive, sensory seeking, and repetitive/stereotypic. Results indicated that hyperresponsive behaviors were most associated with activities of daily living and family-initiated stimuli, whereas sensory seeking behaviors were associated with free play activities and child-initiated stimuli. Behaviors associated with multiple sensory modalities simultaneously were common, emphasizing the multi-sensory nature of children’s behaviors in natural contexts. Implications for future research more explicitly considering context are discussed.
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8. Kuiper MW, Verhoeven EW, Geurts HM. {{The role of interstimulus interval and « Stimulus-type » in prepotent response inhibition abilities in people with ASD: A quantitative and qualitative review}}. {Autism Res}. 2016.
Autism spectrum disorders (ASD) are associated with prepotent response inhibition difficulties. However, the large variation between studies suggests that understudied factors, such as interstimulus interval (ISI) and « stimulus-type » (both hypothesized proxies of stressors influencing arousal), might influence the inhibitory abilities of people with ASD. Using meta-analysis, we tested whether differences in prepotent response inhibition between people with and without ASD was influenced by ISI. There was not enough variation in « stimulus-type » between the studies to include it as a moderator. Thirty-seven studies met inclusion criteria, with a combined sample size of 950 people with ASD and 966 typically developing controls. Additionally, a qualitative review including studies comparing a neutral and an arousing condition in one experiment was performed to examine whether fast ISI or specific arousing stimuli directly influence prepotent response inhibition. The meta-analysis indicated that ISI was not a relevant moderator. The qualitative review showed that ISI and « stimulus-type » had the same effect for both groups. Although all studies regarding ISI indicated that fast ISI worsened performance, different types of stimuli had either a positive or a negative influence. This could suggest that distinctive stimuli might affect arousal differently. While we replicated the inhibition difficulties in people with ASD (g = .51), our results do not show strong ASD-specific effects of ISI or « stimulus-type » on inhibition. Nonetheless, ISI and « stimulus-type » do seem to influence performance. Future research focusing on potential underlying factors (e.g., baseline physiological arousal) is needed to examine why this is the case. Autism Res 2016,. (c) 2016 International Society for Autism Research, Wiley Periodicals, Inc.
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9. Monyak RE, Emerson D, Schoenfeld BP, Zheng X, Chambers DB, Rosenfelt C, Langer S, Hinchey P, Choi CH, McDonald TV, Bolduc FV, Sehgal A, McBride SM, Jongens TA. {{Insulin signaling misregulation underlies circadian and cognitive deficits in a Drosophila fragile X model}}. {Mol Psychiatry}. 2016.
Fragile X syndrome (FXS) is an undertreated neurodevelopmental disorder characterized by low intelligence quotent and a wide range of other symptoms including disordered sleep and autism. Although FXS is the most prevalent inherited cause of intellectual disability, its mechanistic underpinnings are not well understood. Using Drosophila as a model of FXS, we showed that select expression of dfmr1 in the insulin-producing cells (IPCs) of the brain was sufficient to restore normal circadian behavior and to rescue the memory deficits in the fragile X mutant fly. Examination of the insulin signaling (IS) pathway revealed elevated levels of Drosophila insulin-like peptide 2 (Dilp2) in the IPCs and elevated IS in the dfmr1 mutant brain. Consistent with a causal role for elevated IS in dfmr1 mutant phenotypes, the expression of dfmr1 specifically in the IPCs reduced IS, and genetic reduction of the insulin pathway also led to amelioration of circadian and memory defects. Furthermore, we showed that treatment with the FDA-approved drug metformin also rescued memory. Finally, we showed that reduction of IS is required at different time points to rescue circadian behavior and memory. Our results indicate that insulin misregulation underlies the circadian and cognitive phenotypes displayed by the Drosophila fragile X model, and thus reveal a metabolic pathway that can be targeted by new and already approved drugs to treat fragile X patients.Molecular Psychiatry advance online publication, 19 April 2016; doi:10.1038/mp.2016.51.
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10. Napoli E, Song G, Wong S, Hagerman R, Giulivi C. {{Altered Bioenergetics in Primary Dermal Fibroblasts from Adult Carriers of the FMR1 Premutation Before the Onset of the Neurodegenerative Disease Fragile X-Associated Tremor/Ataxia Syndrome}}. {Cerebellum}. 2016.
Fragile X-associated tremor/ataxia syndrome (FXTAS) is a late onset neurodegenerative disorder, characterized by tremors, ataxia, impaired coordination, and cognitive decline. While all FXTAS individuals are carriers of a 55-200 CGG expansion at the 5′-UTR of the fragile X mental retardation gene (FMR1), also known as premutation, not all carriers develop FXTAS symptoms and some display other types of psychological/emotional disorders (e.g., autism, anxiety). The goal of this study was to investigate whether the mitochondrial dysfunction previously observed in fibroblasts from older premutation individuals (>60 years) was already present in younger (17-48 years), non-FXTAS-affected carriers and to identify the type and severity of the bioenergetic deficit. Since FXTAS affects mostly males, while females account for a small part of the FXTAS-affected population displaying less severe symptoms, only fibroblasts from males were evaluated in this study. Based on polarographic and enzymatic measurements, a generalized OXPHOS deficit was noted accompanied by increases in the matrix biomarker citrate synthase, oxidative stress (as increased mtDNA copy number and deletions), and mitochondrial network disruption/disorganization. Some of the outcomes (ATP-linked oxygen uptake, coupling, citrate synthase activity, and mitochondrial network organization) strongly correlated with the extent of the CGG expansion, with more severe deficits observed in cell lines carrying higher CGG number. Furthermore, mitochondrial outcomes can identify endophenotypes among carriers and are robust predictors of the premutation diagnosis before the onset of FXTAS, with the potential to be used as markers of prognosis and/or as readouts of pharmacological interventions.
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11. Navon D, Eyal G. {{Looping Genomes: Diagnostic Change and the Genetic Makeup of the Autism Population}}. {AJS}. 2016; 121(5): 1416-71.
This article builds on Hacking’s framework of « dynamic nominalism » to show how knowledge about biological etiology can interact with the « kinds of people » delineated by diagnostic categories in ways that « loop » or modify both over time. The authors use historical materials to show how « geneticization » played a crucial role in binding together autism as a biosocial community and how evidence from genetics research later made an important contribution to the diagnostic expansion of autism. In the second part of the article, the authors draw on quantitative and qualitative analyses of autism rates over time in several rare conditions that are delineated strictly according to genomic mutations in order to demonstrate that these changes in diagnostic practice helped to both increase autism’s prevalence and create its enormous genetic heterogeneity. Thus, a looping process that began with geneticization and involved the social effects of genetics research itself transformed the autism population and its genetic makeup.
12. Paynter JM, Ferguson S, Fordyce K, Joosten A, Paku S, Stephens M, Trembath D, Keen D. {{Utilisation of evidence-based practices by ASD early intervention service providers}}. {Autism}. 2016.
A number of autism intervention practices have been demonstrated to be effective. However, the use of unsupported practices persists in community early intervention settings. Recent research has suggested that personal, professional and workplace factors may influence intervention choices. The aim of this research was to investigate knowledge and use of strategies, organisational culture, individual attitudes, sources of information and considerations informing intervention choices by early intervention providers. An online survey was completed by 72 early intervention providers from four organisations across Australia. Providers reported high levels of trust and access of information from internal professional development, therapists and external professional development. A range of considerations including child factors, family values and research were rated as important in informing intervention choices. Participants reported greater knowledge and use of evidence-based and emerging practices than unsupported. Levels of use were linked to levels of knowledge, as well as some organisational and attitudinal factors. Areas for future research and implications are discussed.
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13. Perez C, Sawmiller D, Tan J. {{The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation}}. {Neural Dev}. 2016; 11(1): 11.
Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. ASDs are accompanied with substantial economic and emotional cost. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Of particular interest is its role in the Slit/Robo pathway. The Slit/Robo pathway is known to be involved in the regulation of axonal guidance and dendritic spine formation. HS mediates the Slit/Robo interaction; without its presence Slit’s repulsive activity is abrogated. Slit/Robo regulates dendritic spine formation through its interaction with srGAPs (slit-robo GTPase Activating Proteins), which leads to downstream signaling, actin cytoskeleton depolymerization and dendritic spine collapse. Through interference with this pathway, HS deficiency can lead to excess spine formation.
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14. Schuh JM, Eigsti IM, Mirman D. {{Discourse comprehension in autism spectrum disorder: Effects of working memory load and common ground}}. {Autism Res}. 2016.
Pragmatic language impairments are nearly universal in autism spectrum disorders (ASD). Discourse requires that we monitor information that is shared or mutually known, called « common ground. » While many studies have examined the role of Theory of Mind (ToM) in such impairments, few have examined working memory (WM). Common ground impairments in ASD could reflect limitations in both WM and ToM. This study explored common ground use in youth ages 8-17 years with high-functioning ASD (n = 13) and typical development (n = 22); groups did not differ on age, gender, IQ, or standardized language. We tracked participants’ eye movements while they performed a discourse task in which some information was known only to the participant (e.g., was privileged; a manipulation of ToM). In addition, the amount of privileged information varied (a manipulation of WM). All participants were slower to fixate the target when considering privileged information, and this effect was greatest during high WM load trials. Further, the ASD group was more likely to fixate competing (non-target) shapes. Predictors of fixation patterns included ASD symptomatology, language ability, ToM, and WM. Groups did not differ in ToM. Individuals with better WM fixated the target more rapidly, suggesting an association between WM capacity and efficient discourse. In addition to ToM knowledge, WM capacity constrains common ground representation and impacts pragmatic skills in ASD. Social impairments in ASD are thus associated with WM capacity, such that deficits in domain-general, nonsocial processes such as WM exert an influence during complex social interactions. Autism Res 2016. (c) 2016 International Society for Autism Research, Wiley Periodicals, Inc.
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15. Tavares PP, Mouga SS, Oliveira GG, Castelo-Branco M. {{Preserved face inversion effects in adults with autism spectrum disorder: an event-related potential study}}. {Neuroreport}. 2016.
Individuals with autism spectrum disorder (ASD) are impaired in face recognition and emotional expression identification. According to current models, there are at least three levels of face processing: first order (two eyes, above a nose, which is above a mouth), second order (the relative distance between features), and holistic (ability to recognize as faces images that lack distinctive facial features). Some studies have reported deficits in configural and holistic processing in individuals with ASD. We investigated the neural correlates of these phenomena by measuring event-related potentials in high-functioning adults with ASD and healthy controls, during a face decision task, using a comprehensive set of photographic, schematic and Mooney upright and inverted faces, and scrambled images. Behaviorally, ASD and healthy controls were performance matched. At the electrophysiological level, individuals with ASD showed a bilateral N170 inversion effect in latency and left lateralized in amplitude for photographic faces, with bilaterally longer latencies and left higher amplitudes (more negative) N170 for inverted than upright photographic faces, and a right lateralized N170 inversion effect in latency for schematic faces. We conclude that under performance-matched conditions, adults with ASD show preserved N170 inversion effects and associated sparing of facial configural processing. An oral presentation of this work can be consulted using the following link, Supplemental digital content 1, http://links.lww.com/WNR/A382.
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16. Wang L, Jia J, Zhang J, Li K. {{Serum levels of SOD and risk of autism spectrum disorder: A case-control study}}. {Int J Dev Neurosci}. 2016.
Background Autism is a severe developmental disorder with poorly understood etiology. This study examined the clinical significance of serum superoxide dismutase (SOD) level, a marker of oxidative stress, in children with autism spectrum disorder (ASD) and typically-developing children between the ages of 2 and 6 years. METHODS: Ninety-six children diagnosed with ASD and 96 sex and age matched typically-developing children were assessed for serum levels of SOD at admission. S0D were assayed by colorimetry, and severity of ASD was evaluated with the Childhood Autism Rating Scale (CARS) Score. The influence of serum SOD levels on ASD was performed by conditional logistic regression analysis, which allows adjustment for confounding factors. RESULTS: The median serum SOD levels were significantly (P<0.001) lower in children with ASD as compared to typically-developing children [146 (IQR: 133-165) U/ml and 180 (168-199) U/ml, respectively]. Levels of SOD increased with decreasing severity of ASD as defined by the CARS score (r=-0.432, P<0.0001). After adjusting for all other possible covariates, SOD remained can be seen as an independent indictor of ASD with an adjusted odds ratio (OR) of 0.955 (95% confidence interval [CI], 0.942-0.969; P<0.001). Based on the receiver operating characteristic (ROC) curve, the optimal cutoff value of serum level of SOD as an indicator for auxiliary diagnosis of ASD was projected to be 160U/ml, which yielded a sensitivity of 84.7% and a specificity of 71.4%, with the area under the curve at 0.811 (95%CI, 0.747-0.874). CONCLUSIONS: Our data suggests that the decreased serum SOD levels could be implicated in the pathophysiology and progression of autism in Chinese children and can be used as an independent risk indicator of ASD. Lien vers le texte intégral (Open Access ou abonnement)
17. Zaidman-Zait A, Mirenda P, Duku E, Vaillancourt T, Smith IM, Szatmari P, Bryson S, Fombonne E, Volden J, Waddell C, Zwaigenbaum L, Georgiades S, Bennett T, Elsabaggh M, Thompson A. {{Impact of personal and social resources on parenting stress in mothers of children with autism spectrum disorder}}. {Autism}. 2016.
This study examined the longitudinal associations between child behavior problems, coping strategies, social resources, and parenting stress in mothers of young children with autism spectrum disorder. Participants were 283 mothers who completed self- and child-report measures at the time of diagnosis and 2 years later. Hierarchical multiple regression was conducted to predict overall parenting stress. At diagnosis, the final model indicated that high levels of social support and mothers’ use of active engaged coping strategies were associated with lower levels of parenting stress. Conversely, high levels of child externalizing behavior problems, family dysfunction, and mothers’ use of disengaged coping strategies were associated with higher parenting stress. Two years later, high levels of parenting stress at diagnosis predicted increased parenting stress. In addition, high or increasing levels of social support predicted a decrease in parenting stress, while high or increasing levels of family dysfunction predicted increased stress. Finally, increased use of disengaged coping strategies and decreased use of active coping strategies over time predicted higher levels of parenting stress. Results are discussed in terms of their implications for the provision of targeted supports that are designed to enhance the personal and social resources available to mothers of children with autism spectrum disorder.
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18. Zerbo O, Traglia M, Yoshida C, Heuer LS, Ashwood P, Delorenze GN, Hansen RL, Kharrazi M, Van de Water J, Yolken RH, Weiss LA, Croen LA. {{Maternal mid-pregnancy C-reactive protein and risk of autism spectrum disorders: the early markers for autism study}}. {Transl Psychiatry}. 2016; 6: e783.
Maternal pregnancy levels of the inflammatory marker C-reactive protein (CRP) has been previously associated with autism spectrum disorder (ASD) in the offspring. We conducted a population-based nested case-control study with 500 children with ASD, 235 with developmental delay (DD) and 580 general population (GP) controls to further investigate whether elevated CRP during pregnancy increases the risk of ASD. Maternal CRP concentration was measured in archived serum collected during 15-19 weeks of pregnancy and genome-wide single-nucleotide polymorphism (SNP) data were generated. The levels of CRP were compared between ASD vs GP and DD vs GP. The genetic associations with CRP were assessed via linear regression. Maternal CRP levels in mid-pregnancy were lower in mothers of ASD compared with controls. The maternal CRP levels in the upper third and fourth quartiles were associated with a 45 and 44% decreased risk of ASD, respectively. Two SNPs at the CRP locus showed strong association with CRP levels but they were not associated with ASD. No difference was found between maternal CRP levels of DD and controls. The reasons for the lower levels of CRP in mothers of ASD are not known with certainty but may be related to alterations in the immune response to infectious agents. The biological mechanisms underlying this association remain to be clarified.
