Microarchitecture osseuse chez des adolescents garçons avec un trouble du spectre de l'autisme

Traduction partielle: G.M.

Bone. 2017 Jan 11. pii: S8756-3282(17)30009-1. doi: 10.1016/j.bone.2017.01.009.

Bone microarchitecture in adolescent boys with autism spectrum disorder

Neumeyer AM¹, Sokoloff NC², McDonnell E³, Macklin EA⁴, McDougle CJ⁵, Misra M⁶.

Author information

• ¹Lurie Center for Autism, Massachusetts General Hospital, Lexington, MA 02421, United States; Harvard Medical School, Boston, MA 02115, United States. Electronic address: aneumeyer@mgh.harvard.edu
• ²Lurie Center for Autism, Massachusetts General Hospital, Lexington, MA 02421, United States.
• ³Biostatistics Center, Massachusetts General Hospital, Boston, MA 02114, United States.
• ⁴Harvard Medical School, Boston, MA 02115, United States; Biostatistics Center, Massachusetts General Hospital, Boston, MA 02114, United States.
• ⁵Lurie Center for Autism, Massachusetts General Hospital, Lexington, MA 02421, United States; Harvard Medical School, Boston, MA 02115, United States.
• ⁶Harvard Medical School, Boston, MA 02115, United States; Pediatric Endocrine and Neuroendocrine Units, Massachusetts General Hospital, Boston, MA 02114, United States.

Abstract

BACKGROUND:

Les garçons avec trouble du spectre de l'autisme (TSA) ont une densité minérale osseuse de surface (DMOs) inférieure à celle des témoins qui développent typiquement (DT). Des études sur la DMO volumétrique (MDOv) et sur la microarchitecture osseuse fournissent des informations sur le risque de fracture au-delà de celles fournies par la DMOs mais manquent actuellement dans le TSA.
Boys with autism spectrum disorder (ASD) have lower areal bone mineral density (aBMD) than typically developing controls (TDC). Studies of volumetric BMD (vBMD) and bone microarchitecture provide information about fracture risk beyond that provided by aBMD but are currently lacking in ASD.

OBJECTIVES:

To assess ultradistal radius and distal tibia vBMD, bone microarchitecture and strength estimates in adolescent boys with ASD compared to TDC.

DESIGN/METHODS:

Cross-sectional study of 34 boys (16 ASD, 18 TDC) that assessed (i) aBMD at the whole body (WB), WB less head (WBLH), hip and spine using dual X-ray absorptiometry (DXA), (ii) vBMD and bone microarchitecture at the ultradistal radius and distal tibia using high-resolution peripheral quantitative CT (HRpQCT), and (iii) bone strength estimates (stiffness and failure load) using micro-finite element analysis (FEA). We controlled for age in all groupwise comparisons of HRpQCT and FEA measures. Activity questionnaires, food records, physical exam, and fasting levels of 25(OH) vitamin D and bone markers (C-terminal collagen crosslinks and N-terminal telopeptide (CTX and NTX) for bone resorption, N-terminal propeptide of Type 1 procollagen (P1NP) for bone formation) were obtained.

RESULTS:

ASD participants were slightly younger than TDC participants (13.6 vs. 14.2years, p=0.44). Tanner stage, height Z-scores and fasting serum bone marker levels did not differ between groups. ASD participants had higher BMI Z-scores, percent body fat, IGF-1 Z-scores, lower lean mass and aBMD Z-scores than TDC at the WB, WBLH, and femoral neck (P<0.1). At the radius, ASD participants had lower trabecular thickness (0.063 vs. 0.070mm, p=0.004), compressive stiffness (56.7 vs. 69.7kN/mm, p=0.030) and failure load (3.0 vs. 3.7kN, p=0.031) than TDC. ASD participants also had 61% smaller cortical area (6.6 vs. 16.4mm², p=0.051) and thickness (0.08 vs. 0.22mm, p=0.054) compared to TDC. At the tibia, ASD participants had lower compressive stiffness (183 vs. 210kN/mm, p=0.048) and failure load (9.4 vs. 10.8kN, p=0.043) and 23% smaller cortical area (60.3 vs. 81.5mm², p=0.078) compared to TDC. A lower proportion of ASD participants were categorized as "very physically active" (20% vs. 72%, p=0.005). Differences in physical activity, calcium intake and IGF-1 responsiveness may contribute to group differences in stiffness and failure load.

CONCLUSION:

Les paramètres micro-architecturaux osseux sont altérés dans le TSA, avec des réductions des estimations de la résistance osseuse (rigidité et rupture de charge) au niveau du radius ultradistal et du tibia distal. Cela peut résulter d'une diminution de l'activité physique et de l'apport en calcium, et d'une diminution de la sensibilité à l'IGF-1.
Bone microarchitectural parameters are impaired in ASD, with reductions in bone strength estimates (stiffness and failure load) at the ultradistal radius and distal tibia. This may result from lower physical activity and calcium intake, and decreased IGF-1 responsiveness.

Copyright © 2016. Published by Elsevier Inc.

PMID: 28088646

DOI: 10.1016/j.bone.2017.01.009

L'influence du génotype du transporteur 5-HTTLPR sur la connectivité du cortex cingulaire antérieur subgénale de l'amygdale dans le trouble du spectre de l'autisme

Dev Cogn Neurosci. 2016 Dec 23;24:12-20. doi: 10.1016/j.dcn.2016.12.002.

The influence of 5-HTTLPR transporter genotype on amygdala-subgenual anterior cingulate cortex connectivity in autism spectrum disorder

Velasquez F¹, Wiggins JL², Mattson WI², Martin DM³, Lord C⁴, Monk CS⁵.

Author information

• ¹Department of Psychology, University of Michigan, United States. Electronic address: velasqfr@umich.edu.
• ²Department of Psychology, University of Michigan, United States.
• ³Department of Human Genetics, University of Michigan, United States.
• ⁴Center for Autism and the Developing Brain, Weill Cornell Medicine, United States.
• ⁵Department of Psychology, Neuroscience Program, Department of Psychiatry, Center for Growth and Human Development, University of Michigan, United States.

Abstract

Social deficits in autism spectrum disorder (ASD) are linked to amygdala functioning and functional connection between the amygdala and subgenual anterior cingulate cortex (sACC) is involved in the modulation of amygdala activity. Impairments in behavioral symptoms and amygdala activation and connectivity with the sACC seem to vary by serotonin transporter-linked polymorphic region (5-HTTLPR) variant genotype in diverse populations. The current preliminary investigation examines whether amygdala-sACC connectivity differs by 5-HTTLPR genotype and relates to social functioning in ASD. A sample of 108 children and adolescents (44 ASD) completed an fMRI face-processing task. Youth with ASD and low expressing 5-HTTLPR genotypes showed significantly greater connectivity than youth with ASD and higher expressing genotypes as well as typically developing (TD) individuals with both low and higher expressing genotypes, in the comparison of happy vs. baseline faces and happy vs. neutral faces. Moreover, individuals with ASD and higher expressing genotypes exhibit a negative relationship between amygdala-sACC connectivity and social dysfunction. Altered amygdala-sACC coupling based on 5-HTTLPR genotype may help explain some of the heterogeneity in neural and social function observed in ASD. This is the first ASD study to combine genetic polymorphism analyses and functional connectivity in the context of a social task.

Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.

KEYWORDS:

5-HTTLPR; Amygdala; Autism spectrum disorder; Connectivity; Face-processing; Heterogeneity; Serotonin; Subgenual anterior cingulate cortex

PMID: 28088648

DOI: 10.1016/j.dcn.2016.12.002

La nature sociale de la surimitation: aperçus pour l'autisme et le syndrome de Williams

Traduction partielle : G.M.

Cognition. 2017 Jan 12;161:10-18. doi: 10.1016/j.cognition.2017.01.008.

The social nature of overimitation: Insights from Autism and Williams syndrome

Vivanti G¹, Hocking DR², Fanning P³, Dissanayake C³.

Author information

• ¹A.J. Drexel Autism Institute, Drexel University, 3020 Market Street, Suite 560, Philadelphia, PA 19104-3734, USA; Olga Tennison Autism Research Centre, School of Psychology and Public Health, La Trobe University, Bundoora, VIC 3086, Australia. Electronic address: giacomo.vivanti@drexel.edu
• ²Developmental Neuromotor & Cognition Lab, School of Psychology & Public Health, La Trobe University, Australia.
• ³Olga Tennison Autism Research Centre, School of Psychology and Public Health, La Trobe University, Bundoora, VIC 3086, Australia.

Abstract

Lors de l'imitation d'actions nouvelles, les enfants d'âge préscolaire avec un développement typique  copient souvent des composantes de la démonstration qui ne sont pas liées à l'objectif de l'action modélisée, phénomène connu sous le nom de «surimitation».
 When imitating novel actions, typically developing preschoolers often copy components of the demonstration that are unrelated to the modeled action's goal, a phenomenon known as 'overimitation'. 
According to the social motivation account, overimitation fulfills social affiliation motives (i.e., the imitator's drive to experience social connectedness with the demonstrator and the social context). Conversely, according to the social-cognitive account, overimitation reflects overattribution of causal relevance (i.e., the imitator's failure to appreciate that some components of the demonstration are not relevant to the action's outcome). Autism Spectrum Disorder (ASD) and William syndrome (WS) are characterized by reduced and enhanced spontaneous social motivation, respectively, as well as similar impairments in social-cognition, thus providing helpful test cases to understand the nature of overimitation. Using a novel eye-tracking paradigm, we examined overimitation in 31 preschoolers with ASD, 18 age- and IQ-matched peers with WS, and 19 age-matched typically developing children.
Nous avons constaté que les enfants avec un syndrome de Williams et les enfants avec un développement typique étaient plus susceptibles de surimiter et d'attirer leur attention sur le visage du modèle lors de la démonstration d'actions causales non pertinentes par rapport à ceux avec TSA.
We found that children with WS and typically developing children were more likely to overimitate, and to increase their attention to the model's face during demonstration of causally irrelevant actions, compared to those with ASD.  
These findings will be discussed in the context of support for the social-motivational account of overimitation.

Copyright © 2017 Elsevier B.V. All rights reserved.

KEYWORDS: Autism; Imitation; Overimitation; Social learning; Williams syndrome

PMID: 28088702

DOI: 10.1016/j.cognition.2017.01.008