Pubmed du 11/10/19

vendredi 11 octobre 2019

1. Bodner KE, Cowan N, Christ SE. Contributions of filtering and attentional allocation to working memory performance in individuals with autism spectrum disorder. J Abnorm Psychol ;2019 (Oct 10)

Past findings on working memory (WM) ability in individuals with autism spectrum disorder (ASD) are mixed. The present objective was to assess not only the integrity of WM capacity, but also the potential contribution of filtering ability and attentional selection to WM performance, in individuals with ASD. A sample of 24 participants with ASD (Mage = 19.6 years) and 24 typically developing participants without ASD (Mage = 20.3 years) participated. Participants completed a computerized paradigm designed to systematically assess WM capacity, visual filtering ability, and attentional selection. In brief, participants were shown visual arrays consisting of 2-8 colored stimuli (circles and/or squares). After a short delay, memory for one of the stimuli was probed. Importantly, participants were informed beforehand that one of the shape types (e.g., circles) was more likely to be probed compared to the other shape type (e.g., squares) - thus making it strategically advantageous to focus on the high frequency shapes and to filter/ignore the low frequency shapes. Eye tracking data were simultaneously collected. The ASD group demonstrated intact WM capacity and filtering ability, but disrupted ability to efficiently allocate capacity under the demands of high WM load. Analysis of eye tracking data suggests the groups may have differed in their strategic approach to encoding stimuli which may have, in turn, contributed to the aforementioned impairment. Findings support the assertion that disruptions in secondary processes such as strategy use and attentional selection may have played a role in previous reports of WM impairment in ASD. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

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2. Guo X, Duan X, Chen H, He C, Xiao J, Han S, Fan YS, Guo J. Altered inter- and intrahemispheric functional connectivity dynamics in autistic children. Hum Brain Mapp ;2019 (Oct 10)

Emerging evidence has associated autism spectrum disorder (ASD) with static functional connectivity abnormalities between multiple brain regions. However, the temporal dynamics of intra- and interhemispheric functional connectivity patterns remain unknown in ASD. Resting-state functional magnetic resonance imaging data were analyzed for 105 ASD and 102 demographically matched typically developing control (TC) children (age range : 7-12 years) available from the Autism Brain Imaging Data Exchange database. Whole-brain functional connectivity was decomposed into ipsilateral and contralateral functional connectivity, and sliding-window analysis was utilized to capture the intra- and interhemispheric dynamic functional connectivity density (dFCD) patterns. The temporal variability of the functional connectivity dynamics was further quantified using the standard deviation (SD) of intra- and interhemispheric dFCD across time. Finally, a support vector regression model was constructed to assess the relationship between abnormal dFCD variance and autism symptom severity. Both intra- and interhemispheric comparisons showed increased dFCD variability in the anterior cingulate cortex/medial prefrontal cortex and decreased variability in the fusiform gyrus/inferior temporal gyrus in autistic children compared with TC children. Autistic children additionally showed lower intrahemispheric dFCD variability in sensorimotor regions including the precentral/postcentral gyrus. Moreover, aberrant temporal variability of the contralateral dFCD predicted the severity of social communication impairments in autistic children. These findings demonstrate altered temporal dynamics of the intra- and interhemispheric functional connectivity in brain regions incorporating social brain network of ASD, and highlight the potential role of abnormal interhemispheric communication dynamics in neural substrates underlying impaired social processing in ASD.

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3. Hamner T, Hepburn S, Zhang F, Fidler D, Robinson Rosenberg C, Robins DL, Lee NR. Cognitive Profiles and Autism Symptoms in Comorbid Down Syndrome and Autism Spectrum Disorder. J Dev Behav Pediatr ;2019 (Oct 8)

OBJECTIVE : The prevalence of comorbid autism spectrum disorder (ASD) in children with Down syndrome (DS) is estimated to be around 16%. This study aims to fill gaps in the literature by describing developmental and behavioral phenotypes in this group relative to those with DS or ASD in isolation. METHODS : Participants included 173 children (Mage = 73 months) with ASD, DS, or DS + ASD. Two 3 x 2 repeated-measures analyses of variance were completed with between-subject factors of the diagnostic group (DS, ASD, and DS + ASD) and within-subject factors of cognitive performance (verbal and nonverbal developmental quotient [DQ]) or ASD symptoms (social affect [SA] and restricted and repetitive behaviors [RRBs]). RESULTS : Significant group-by-scale interactions were found, and pairwise comparisons revealed that for verbal DQ, DS + ASD < DS, ASD, whereas for nonverbal DQ, DS + ASD < DS < ASD. For SA, DS < DS + ASD < ASD, whereas for RRB, DS, DS + ASD < ASD. CONCLUSION : Findings suggest greater cognitive impairment in DS + ASD on both verbal and nonverbal measures. Despite these significant cognitive challenges, ASD symptoms appeared less severe in DS + ASD relative to peers with ASD in isolation, although SA symptoms were elevated over DS-only. This unique DS + ASD presentation has important implications for early identification and intervention. Given previous research suggesting relative social strengths in DS and less severe ASD symptoms documented in this study, future research may benefit from investigating different aspects of SA (i.e., components related to reciprocal social interaction vs. social communication) in those with DS + ASD to more clearly delineate the social phenotype in this group and potentially inform intervention efforts.

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4. Hegarty IJ, Lazzeroni LC, Raman MM, Hallmayer JF, Cleveland SC, Wolke ON, Phillips JM, Reiss AL, Hardan AY. Genetic and environmental influences on corticostriatal circuits in twins with autism. J Psychiatry Neurosci ;2019 (Oct 11) ;44(6):190030.

Background : Corticostriatal circuits (CSC) have been implicated in the presentation of some restricted and repetitive behaviours (RRBs) in children with autism-spectrum disorder (ASD), and preliminary evidence suggests that disruptions in these pathways may be associated with differences in genetic and environmental influences on brain development. The objective of this investigation was to examine the impact of genetic and environmental factors on CSC regions in twins with and without ASD and to evaluate their relationship with the severity of RRBs. Methods : We obtained T1-weighted MRIs from same-sex monozygotic and dizygotic twin pairs, aged 6-15 years. Good-quality data were available from 48 ASD pairs (n = 96 twins ; 30 pairs concordant for ASD, 15 monozygotic and 15 dizygotic ; 18 pairs discordant for ASD, 4 monozygotic and 14 dizygotic) and 34 typically developing control pairs (n = 68 twins ; 20 monozygotic and 14 dizygotic pairs). We generated structural measures of the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), caudate, putamen, pallidum and thalamus using FreeSurfer. Twin pair comparisons included intraclass correlation analyses and ACE modelling (a2 = additive genetics ; c2 = common or shared environment ; e2 = unique or nonshared environment). We also assessed correlations with RRB severity. Results : Structural variation in CSC regions was predominantly genetically mediated in typically developing twins (a2 = 0.56 to 0.87), except for ACC white matter volume (a2 = 0.42, 95% confidence interval [CI] 0.08 to 0.77). We also observed similar magnitudes of genetic influence in twins with ASD (a2 = 0.65 to 0.97), but the cortical thickness of the ACC (c2 = 0.44, 95% CI 0.22 to 0.66) and OFC (c2 = 0.60, 95% CI 0.25 to 0.95) was primarily associated with environmental factors in only twins with ASD. Twin pair differences in OFC grey matter volume were also correlated with RRB severity and were predominantly environmentally mediated. Limitations : We obtained MRIs on 2 scanners, and analytical approaches could not identify specific genetic and environmental factors. Conclusion : Genetic factors primarily contribute to structural variation in subcortical CSC regions, regardless of ASD, but environmental factors may exert a greater influence on the development of grey matter thickness in the OFC and ACC in children with ASD. The increased vulnerability of OFC grey matter to environmental influences may also mediate some heterogeneity in RRB severity in children with ASD.

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5. Kohli JS, Kinnear MK, Martindale IA, Carper RA, Muller RA. Regionally decreased gyrification in middle-aged adults with autism spectrum disorders. Neurology ;2019 (Oct 11)

OBJECTIVE : To examine changing features of cortical morphology in middle-aged adults with autism spectrum disorders (ASDs) vs typical comparison (TC) participants, hypothesizing regionally decreased local gyrification index (lGI), given our previous findings of accelerated lGI decline during adolescence. METHODS : After quality assurance, T1-weighted MRI sequences from 20 participants with ASD and 21 TC participants (40-61 years) matched on age were analyzed. lGI, cortical thickness (CT), and surface area (SA) were measured with FreeSurfer version 5.3. Statistical analyses used a general linear model including age, nonverbal IQ, and total brain volume as covariates. Clusters of significant group effects were used as regions of interest for behavioral analyses. RESULTS : Clusters of decreased lGI were observed bilaterally in the ASD group with large effect sizes in insular and anterior cingulate (ACC), left postcentral, and middle frontal and right orbitofrontal and supramarginal regions. lGI was also shown to decline with age across groups in bilateral precentral and right supramarginal clusters. No significant group, age, or group-by-age interaction effects were observed for CT or SA in this age group. lGI showed a significant correlation with Social Responsiveness Scale total scores in a right caudal ACC cluster in the TC group only, while several correlations were found in the ASD group between executive function scores and clusters in the bilateral insula and right orbitofrontal cortex. CONCLUSION : The pattern of regionally decreased lGI observed here in middle-aged adults with ASDs is consistent with an abnormal trajectory of cortical folding changes across different stages of life in ASDs, as shown in previous studies.

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6. Lane C, Robinson L, Freeth M. Autistic traits and cognitive abilities associated with two molecular causes of Silver-Russell syndrome. J Abnorm Psychol ;2019 (Oct 10)

Silver-Russell syndrome is a rare genetic imprinting disorder. Two molecular causes of Silver-Russell syndrome have been identified : loss of methylation on chromosome 11p15 (11p15 LOM) and maternal uniparental disomy for chromosome 7 (matUPD7). Current understanding of the cognitive and behavioral phenotypes associated with these two molecular subtypes is limited. This study aimed to address this gap in the literature. The Social Responsiveness Scale (SRS-2) was used to assess autistic traits in individuals with 11p15 LOM (n = 47) and matUPD7 (n = 32). A subset of participants with 11p15 LOM (n = 18) and matUPD7 (n = 15) completed in-person assessments : the Autism Diagnostic Observation Schedule (ADOS-2) and the British Ability Scales (BAS3). Overall, 37.50% of the matUPD7 group and 10.64% of the 11p15 LOM group scored above the SRS-2 severe clinical cut-off. Based on the ADOS-2, 33.33% of the matUPD7 participants and 11.11% of the 11p15 LOM participants scored above cut-off for autism spectrum/autism. Intellectual ability was significantly lower in the matUPD7 group (M = 79.86) compared with the 11p15 LOM group (M = 98.56). However, there was no evidence of an uneven cognitive profile associated with either group or of an association between autistic traits and intellectual ability. Although both 11p15 LOM and matUPD7 have the same clinical diagnosis of Silver-Russell syndrome, there are some differences in the cognitive and behavioral phenotypes between these two molecular subtypes. This has implications for considering access to services, intervention, and support within these populations, particularly in relation to learning and behavior. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

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7. Ma J, Zhang LQ, He ZX, He XX, Wang YJ, Jian YL, Wang X, Zhang BB, Su C, Lu J, Huang BQ, Zhang Y, Wang GY, Guo WX, Qiu DL, Mei L, Xiong WC, Zheng YW, Zhu XJ. Autism candidate gene DIP2A regulates spine morphogenesis via acetylation of cortactin. PLoS Biol ;2019 (Oct) ;17(10):e3000461.

Dendritic spine development is crucial for the establishment of excitatory synaptic connectivity and functional neural circuits. Alterations in spine morphology and density have been associated with multiple neurological disorders. Autism candidate gene disconnected-interacting protein homolog 2 A (DIP2A) is known to be involved in acetylated coenzyme A (Ac-CoA) synthesis and is primarily expressed in the brain regions with abundant pyramidal neurons. However, the role of DIP2A in the brain remains largely unknown. In this study, we found that deletion of Dip2a in mice induced defects in spine morphogenesis along with thin postsynaptic density (PSD), and reduced synaptic transmission of pyramidal neurons. We further identified that DIP2A interacted with cortactin, an activity-dependent spine remodeling protein. The binding activity of DIP2A-PXXP motifs (P, proline ; X, any residue) with the cortactin-Src homology 3 (SH3) domain was critical for maintaining the level of acetylated cortactin. Furthermore, Dip2a knockout (KO) mice exhibited autism-like behaviors, including excessive repetitive behaviors and defects in social novelty. Importantly, acetylation mimetic cortactin restored the impaired synaptic transmission and ameliorated repetitive behaviors in these mice. Altogether, our findings establish an initial link between DIP2A gene variations in autism spectrum disorder (ASD) and highlight the contribution of synaptic protein acetylation to synaptic processing.

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8. McDaniel J, Yoder P, Estes A, Rogers SJ. Validity of Vocal Communication and Vocal Complexity in Young Children with Autism Spectrum Disorder. J Autism Dev Disord ;2019 (Oct 9)

To identify valid measures of vocal development in young children with autism spectrum disorder in the early stages of language learning, we evaluated the convergent validity, divergent validity, and sensitivity to change (across 12 months) of two measures of vocal communication and two measures of vocal complexity through conventional coding of communication samples. Participants included 87 children with autism spectrum disorder (M = 23.42 months at entry). All four vocal variables demonstrated consistent evidence of convergent validity, divergent validity, and sensitivity to change with large effect sizes for convergent validity and sensitivity to change. The results highlight the value of measuring vocal communication and vocal complexity in future studies.

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9. Mundy P. International Society for Autism Research News President’s Message - October 2019. Autism Res ;2019 (Oct) ;12(10):1574.

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