1. {{« Characterizing autism-relevant social behavior in poodles (Canis familiaris) via owner report »: Correction to Zamzow et al. (2017)}}. {J Comp Psychol};2017 (May);131(2):149.
Reports an error in « Characterizing Autism-Relevant Social Behavior in Poodles via Owner Report » by Rachel M. Zamzow, Lisa Lit, Shelley Hamilton and David Q. Beversdorf (Journal of Comparative Psychology, Advanced Online Publication, Mar 13, 2017, np). In the article, the scientific name for the species was missing in the title. All versions of this article have been corrected. (The following abstract of the original article appeared in record 2017-11247-001.) Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by deficits in social communication and the presence of restricted, repetitive behaviors. It can be difficult to model the complex behavioral features of this disorder with rodent models, which have limited similarity to human behaviors. The domestic dog may be a promising model of complex human behavior, including core features of ASD. The present study examines ASD-relevant social behavior in Miniature and Standard Poodles using an owner-report questionnaire with questions adapted from the Autism Diagnostic Observation Schedule (Lord, Rutter, DiLavore, & Risi, 2000). A previous study identified 3 behavioral constructs examined by this questionnaire: initiation of reciprocal social behaviors, response to social interaction, and communication. In the present study, confirmatory and experimental factor analyses used to assess how collected data fit with the previous model revealed moderate model fit and a similar factorial structure. Between-breed comparisons across these factors and at the individual question level revealed differences between Miniature and Standard Poodles in showing behaviors. Cluster analyses used to group dogs within each breed according to social behavior identified smaller subgroups of dogs with less social behavior across all 3 factors compared with the average within each breed. Within- and between-breed differences in social behavior warrant investigation of genetic variation underlying this complex trait as it relates to ASD-relevant behavior. (PsycINFO Database Record
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2. Alhowikan AM, Ayadhi LA, Halepoto DM. {{Secretagogin (SCGN) Plasma Levels and their Association with Cognitive and Social Behavior in Children with Autism Spectrum Disorder ASD)}}. {J Coll Physicians Surg Pak};2017 (Apr);27(4):222-226.
OBJECTIVE: To investigate the secretagogin (SCGN) plasma levels in children with autism spectrum disorder (ASD) compared to age and gender-matched healthy control, and its association with cognitive and social behaviors by using childhood autism rating scale (CARS) and social responsiveness scale (SRS). STUDY DESIGN: Case-control study. PLACE AND DURATION OF STUDY: Autism Research and Treatment Center, Al-Amodi Autism Research Chair, Department of Physiology, Faculty of Medicine, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia, from October 2015 to May 2016. METHODOLOGY: SCGN levels were determined in the plasma of thirty-seven (37) autistic children using enzyme-linked immunosorbent assay (ELISA), categorized as mild-moderate and severe as indicated by their CARS scores and compared with thirty (30) age and gender-matched control samples. Correlation between SCGN levels and different cognitive and social behavior scales (CARS and SRS) was determined by Spearman’s correlation coefficient (r). RESULTS: The results indicated that autistic children (n=37) had significantly (p= 0.005) lower plasma level of SCGN {45.7 (26.2) ng/ml [median (IQR)]} than those of healthy controls {n=30, 70.8 (48.6) ng/ml [median (IQR)]}. Children with severe (n=28, 76%) as well as mild to moderate autism (n=09, 24%) also exhibited significantly lower SCGN levels {47.5 (27) ng/ml [median (IQR)], p =0.014} and {45.7 (16.6) ng/ml [median (IQR)], p = 0.02)}, respectively than healthy controls {n=30, 70.8 (48.6) ng/ml [median (IQR)]}. However, there was no significant difference between the SCGN levels of children with mild to moderate and severe autism (p = 0.66). Spearman’s correlation coefficient (r) was used to determine the relationships between SCGN levels and different variables (CARS, SRS). However, the results showed no significant correlation between SCGN and these scales. (CARS, r=-0.03, p=0.86; SRS, r=0.21, p=0.20). CONCLUSION: The low SCGN plasma levels in children with ASD probably indicate that SCGN might be implicated in the pathogenesis of autism. However, these data should be treated with caution until further investigations are performed using larger sample sizes to determine whether the decrease in plasma SCGN levels is a mere consequence of autism or it plays a pathogenic role in the disease.
3. Bangerter A, Ness S, Aman MG, Esbensen AJ, Goodwin MS, Dawson G, Hendren R, Leventhal B, Khan A, Opler M, Harris A, Pandina G. {{Autism Behavior Inventory: A Novel Tool for Assessing Core and Associated Symptoms of Autism Spectrum Disorder}}. {J Child Adolesc Psychopharmacol};2017 (May 12)
OBJECTIVE: Autism Behavior Inventory (ABI) is a new measure for assessing changes in core and associated symptoms of autism spectrum disorder (ASD) in participants (ages: 3 years-adulthood) diagnosed with ASD. It is a web-based tool with five domains (two ASD core domains: social communication, restrictive and repetitive behaviors; three associated domains: mental health, self-regulation, and challenging behavior). This study describes design, development, and initial psychometric properties of the ABI. METHODS: ABI items were generated following review of existing measures and inputs from expert clinicians. Initial ABI scale contained 161 items that were reduced to fit a factor analytic model, retaining items of adequate reliability. Two versions of the scale, ABI-full (ABI-F; 93 items) and ABI-short version (ABI-S; 36 items), were developed and evaluated for psychometric properties, including validity comparisons with commonly used measures. Both scales were administered to parents and healthcare professionals (HCPs) involved with study participants. RESULTS: Test-retest reliability (intraclass correlation coefficient [ICC] = 0.79) for parent ratings on ABI was robust and compared favorably to existing scales. Test-retest correlations for HCP ratings were generally lower versus parent ratings. ABI core domains and comparison measures strongly correlated (r >/= 0.70), demonstrating good concurrent validity. CONCLUSIONS: Overall, ABI demonstrates promise as a tool for measuring change in core symptoms of autism in ASD clinical studies, with further validation required.
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4. Coleman-Fountain E. {{Uneasy encounters: Youth, social (dis)comfort and the autistic self}}. {Soc Sci Med};2017 (May 12);185:9-16.
Notions of deficit and ‘faultiness’ shape depictions of the association between autism and uneasy social relationships. That framing has been the focus of critique by autistic activists and scholars who, exploring autistic people’s sociality, reframe issues of social difficulty in terms of inequality and discomfort. Located within this set of debates, the article analyses data from a UK based study of mental health narratives derived from semi-structured interviews with 19 autistic young adults aged 23 to 24. The NIHR funded the study, and a UK National Health Service Research Ethics Committee gave ethical approval. Sociality and social difficulties, feelings of discomfort, and perceptions of the autistic self as ‘faulty’ were themes of the study. Exploring the nexus of inequality, non-autistic social power, fears about social performance and (dis)comfort that underpinned the accounts, the article explores the conclusions the young adults reached about social difficulty. Critically examining notions of improvability, the article contributes to debates about sociality, social difficulty and comfort by questioning the assumption that social dysfunction is due to autistic ‘fault’. The article concludes with a discussion of inequality in autistic and non-autistic encounters, and of the social dynamics that deny autistic people social comfort.
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5. Guzik G. {{Early developed ASD (adjacent segmental disease) in patients after surgical treatment of the spine due to cancer metastases}}. {J Orthop Surg Res};2017 (May 12);12(1):70.
BACKGROUND: The causes of ASD are still relatively unknown. Correlation between clinical status of patients and radiological MRI findings is of primary importance. The radiological classifications proposed by Pfirmann and Oner are most commonly used to assess intradiscal degenerative changes. The aim of the study was to assess the influence of the extension of spine fixation on the risk of developing ASD in a short time after surgery. METHODS: A total of 332 patients with spinal tumors were treated in our hospital between 2010 and 2013. Of these patients, 287 underwent surgeries. A follow-up MRI examination was performed 12 months after surgical treatment. The study population comprised of 194 patients. Among metastases, breast cancer was predominant (29%); neurological deficits were detected in 76 patients. Metastases were seen in the thoracic (45%) and lumbar (30%) spine; in 25% of cases, they were of multisegmental character. Pathological fractures concerned 88% of the patients. Statistical calculations were made using the chi2 test. Statistical analysis was done using the Statistica v. 10 software. A p value <0.05 was accepted as statistically significant. The study population was divided on seven groups according to applied treatment. RESULTS: Clinical signs of ASD were noted in only seven patients. Two patients had symptoms of nerve root irritation in the lumbar spine. Twenty-two patients (11%) were diagnosed with ASD according to the MRI classifications by Oner, Rijt, and Ramos, while the more sensitive Pfirmann classification allowed to detect the disease in 46 patients (24%). Healthy or almost healthy discs of Oner type I correlated with the criteria of Pfirmann types II and III. The percentage of the incidence of ASD diagnosed 1 year after the surgery using the Pfirmann classifications was significantly higher than diagnosed according to the clinical examination. CONCLUSIONS: The incidence of ASD in patients after spine surgeries due to cancer metastases does not differ between the study groups. ASD detectability based on clinical signs is significantly lower than ASD detectability based on MR images according to the system by Pfirrmann et.al. ASD risk increase among patients with multilevel fixation. Lien vers le texte intégral (Open Access ou abonnement)
6. May T, Sciberras E, Brignell A, Williams K. {{Autism spectrum disorder: updated prevalence and comparison of two birth cohorts in a nationally representative Australian sample}}. {BMJ Open};2017 (May 09);7(5):e015549.
OBJECTIVES: This study aimed to (1) provide an update on the prevalence of parent-reported autism spectrum disorder (ASD) diagnosis and new information about teacher-reported ASD in two nationally representative Australian cohorts at ages 10-11 years, (2) examine differences in cohort demographic and clinical profiles and (3) compare the prevalence of teacher-reported ASD and any changes in categorisation over time across the cohorts. DESIGN: Secondary analyses were undertaken using data from the Longitudinal Study of Australian Children (LSAC). PARTICIPANTS: Children were recruited at kindergarten age (K cohort; birth year 1999/2000) and birth (B cohort; birth year 2003/2004), with follow-up of every 2 years for six waves. PRIMARY OUTCOME MEASURES: Parent-reported and teacher-reported ASD diagnosis was ascertained at three time points (waves 4-6). RESULTS: At age 10-11 years, the adjusted prevalence of parent-reported ASD diagnosis was 3.9% (95% CI 3.2 to 4.5) and 2.4% (95% CI 1.6 to 2.9) in the B and K cohorts, respectively. Teacher-reported prevalence of ASD was 1.7% (95% CI 1.2 to 2.1) in the B cohort and 0.9% (95% CI 0.56 to 1.14) in the K cohort. Parents reported fewer conduct and peer problems and teachers more pro-social behaviour in B relative to K cohort ASD children. Children reported only by parents in the later-born B cohort had milder behaviour problems than parent-agreed and teacher-agreed cases. Although individual switching to ASD from other categories from 8-9 to 10-11 years was low (K cohort n=5, B cohort n=6), teachers reported more children with ASD in the B than K cohort at 10-11 years and fewer children with emotional/ behavioural problems. CONCLUSIONS: The higher prevalence of parent-reported and teacher-reported ASD diagnosis in the later-born cohort may be partially explained by identifying children with milder behavioural problems as ASD and a change in the use of diagnostic categories in schools.
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7. Sungur AO, Jochner MCE, Harb H, Kilic A, Garn H, Schwarting RKW, Wohr M. {{Aberrant cognitive phenotypes and altered hippocampal BDNF expression related to epigenetic modifications in mice lacking the post-synaptic scaffolding protein SHANK1: Implications for autism spectrum disorder}}. {Hippocampus};2017 (May 12)
Autism spectrum disorder (ASD) is a class of neurodevelopmental disorders characterized by persistent deficits in social communication/interaction, together with restricted/repetitive patterns of behavior. ASD is among the most heritable neuropsychiatric conditions, and while available evidence points to a complex set of genetic factors, the SHANK gene family has emerged as one of the most promising candidates. Here, we assessed ASD-related phenotypes with particular emphasis on social behavior and cognition in Shank1 mouse mutants in comparison to heterozygous and wildtype littermate controls across development in both sexes. While social approach behavior was evident in all experimental conditions and social recognition was only mildly affected by genotype, Shank1-/- null mutant mice were severely impaired in object recognition memory. This effect was particularly prominent in juveniles, not due to impairments in object discrimination, and replicated in independent mouse cohorts. At the neurobiological level, object recognition deficits were paralleled by increased brain-derived neurotrophic factor (BDNF) protein expression in the hippocampus of Shank1-/- mice; yet BDNF levels did not differ under baseline conditions. We therefore investigated changes in the epigenetic regulation of hippocampal BDNF expression and detected an enrichment of histone H3 acetylation at the Bdnf promoter1 in Shank1-/- mice, consistent with increased learning-associated BDNF. Together, our findings indicate that Shank1 deletions lead to an aberrant cognitive phenotype characterized by severe impairments in object recognition memory and increased hippocampal BDNF levels, possibly due to epigenetic modifications. This result supports the link between ASD and intellectual disability, and suggests epigenetic regulation as a potential therapeutic target. This article is protected by copyright. All rights reserved.
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8. Zingale M, Citta S, Occhipinti P, Elia F, Buono S. {{[Neuropsychological profiles, personality features and familial relational patterns in parents of children with Autism Spectrum Disorders]}}. {Riv Psichiatr};2017 (Mar-Apr);52(2):75-82.
INTRODUCTION: The study of neuropsychological profiles and personality features of parents of persons with Autism Spectrum Disorder (ASD) has highlighted specific traits that turned out to be useful for diagnostic purposes. AIM AND METHODS: In our study, psychodiagnostic measures have been used to investigate cognitive profiles, personality features and familial relational patters in a group of parents of children with ASD associated to Intellectual Disability (ID). This group was then compared with a another group of parents of children with Prader-Willi syndrome. RESULTS: Results show no differences between the two groups with regard to Intellectual Quotient, while significant differences were found at the intelligence test Wechsler, which partially confirmed data from the literature relating to the performances of parents of persons with ASD. No differences were found in the executive functioning and memory abilities. As for familial relational patters, families of children with ASD showed decreased cohesion and higher disengagement. DISCUSSION AND CONCLUSIONS: Results obtained in the domains of familial relational patterns and emotional personality components seem to confirm how children’s disability can significantly impact on the entire household, in particular in the case of children with ASD. This data suggest the need for intervention programs aimed at supporting the entire household, with the objective of improving coping strategies and resilience resources of the family.
