Pubmed du 10/06/18

Pubmed du jour

2018-06-10 12:03:50

1. Baron-Mendoza I, Garcia O, Calvo-Ochoa E, Rebollar-Garcia JO, Garzon-Cortes D, Haro R, Gonzalez-Arenas A. {{Alterations in neuronal cytoskeletal and astrocytic proteins content in the brain of the autistic-like mouse strain C58/J}}. {Neurosci Lett}. 2018; 682: 32-8.

Autism spectrum disorder (ASD) is a neurodevelopment disorder characterized by deficient social interaction, impaired communication as well as repetitive behaviors. ASD subjects present connectivity and neuroplasticity disturbances associated with morphological alterations in axons, dendrites, and dendritic spines. Given that the neuronal cytoskeleton and astrocytes have an essential role in regulating several mechanisms of neural plasticity, the aim of this work was to study alterations in the content of neuronal cytoskeletal components actin and tubulin and their associated proteins, as well as astrocytic proteins GFAP and TSP-1 in the brain of a C58/J mouse model of ASD. We determined the expression and regulatory phosphorylation state of cytoskeletal components in the prefrontal cortex, hippocampus, and cerebellum of C58/J mice by means of Western blotting. Our results show that autistic-like mice present: 1) region-dependent altered expression and phosphorylation patterns of Tau isoforms, associated with anomalous microtubule depolymerization; 2) reduced MAP2A content in prefrontal cortex; 3) region-dependent changes in cofilin expression and phosphorylation, associated with abnormal actin filament depolymerizing dynamics; 4) diminished synaptopodin levels in the hippocampus; and 5) reduced content of the astrocyte-secreted protein TSP-1 in the prefrontal cortex and hippocampus. Our work demonstrates changes in the expression and phosphorylation of cytoskeletal proteins as well as in TSP-1 in the brain of the autistic-like mice C58/J, shedding light in one of the possible molecular mechanisms underpinning neuroplasticity alterations in the ASD brain and laying the foundation for future investigations in this topic.

Lien vers le texte intégral (Open Access ou abonnement)

2. Korzeniewski SJ, Allred EN, O’Shea TM, Leviton A, Kuban KCK. {{Elevated protein concentrations in newborn blood and the risks of autism spectrum disorder, and of social impairment, at age 10 years among infants born before the 28th week of gestation}}. {Translational psychiatry}. 2018; 8(1): 115.

Among the 1 of 10 children who are born preterm annually in the United States, 6% are born before the third trimester. Among children who survive birth before the 28th week of gestation, the risks of autism spectrum disorder (ASD) and non-autistic social impairment are severalfold higher than in the general population. We examined the relationship between top quartile inflammation-related protein concentrations among children born extremely preterm and ASD or, separately, a high score on the Social Responsiveness Scale (SRS total score >/=65) among those who did not meet ASD criteria, using information only from the subset of children whose DAS-II verbal or non-verbal IQ was >/=70, who were assessed for ASD, and who had proteins measured in blood collected on >/=2 days (N = 763). ASD (N = 36) assessed at age 10 years is associated with recurrent top quartile concentrations of inflammation-related proteins during the first post-natal month (e.g., SAA odds ratio (OR); 95% confidence interval (CI): 2.5; 1.2-5.3) and IL-6 (OR; 95% CI: 2.6; 1.03-6.4)). Top quartile concentrations of neurotrophic proteins appear to moderate the increased risk of ASD associated with repeated top quartile concentrations of inflammation-related proteins. High (top quartile) concentrations of SAA are associated with elevated risk of ASD (2.8; 1.2-6.7) when Ang-1 concentrations are below the top quartile, but not when Ang-1 concentrations are high (1.3; 0.3-5.8). Similarly, high concentrations of TNF-alpha are associated with heightened risk of SRS-defined social impairment (N = 130) (2.0; 1.1-3.8) when ANG-1 concentrations are not high, but not when ANG-1 concentrations are elevated (0.5; 0.1-4.2).

Lien vers le texte intégral (Open Access ou abonnement)

3. Kumazaki H, Okamoto M, Kanzaki S, Okada KI, Mimura M, Minabe Y, Kikuchi M. {{Approaches for Assessing Olfaction in Children with Autism Spectrum Disorder}}. {Methods in molecular biology (Clifton, NJ)}. 2018; 1820: 221-8.

Olfactory traits in individuals with autism spectrum disorder (ASD) are considered the strongest predictors of social impairment. Compared to other sensory abnormalities, olfactory abnormalities in individuals with ASD are poorly understood. In this chapter, we provide an overview of the current assessment in individuals with ASD. Several confounding factors have to be considered when conducting research on olfaction in individuals with ASD. Qualitative measures of olfaction contain only limited information about the olfactory stimuli. In addition, little systematic information is available about individual’s actual uses of olfaction in daily life. Only a limited number of experimental studies have performed quantitative measurements of olfactory abnormalities in ASD. Therefore, clarifying the relationship between olfactory traits and the influence of real-life situations in a laboratory setting is very difficult. Some new methodologies for measuring olfactory traits are gradually becoming available. New methods that reveal important links between ASD and olfactory traits should be developed in the future.

Lien vers le texte intégral (Open Access ou abonnement)

4. Shao SS, Huang K, Yan SQ, You Y, Pan WJ, Chen X, Cao H, Zhu P, Hao JH, Tao FB. {{[Association between pregnancy-related anxiety of pregnant women and autism-like behavior in their offspring at 18 months of age]}}. {Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi}. 2018; 39(6): 826-9.

Objective: To investigate the relationship of pregnancy-related anxiety of pregnant women in second/third trimesters and autism-like behaviors in their offspring at 18 months of age. Methods: Based on a prospective cohort study design, we evaluated the situation of pregnancy-related anxiety of women during second and third trimesters through a Pregnancy-Related Anxiety Questionnaire. Subjects under study were classified into three groups, 1) those with pregnancy- related anxiety during both trimesters, 2) those with pregnancy-related anxiety at one trimester and 3) those without pregnancy-related anxiety in either trimester. When their children were 18 months, autism-like behaviors (ALB) were evaluated, using the part A of Checklist for Autism in Toddlers-23, and then classified into three groups as non-ALB group, minor ALB group and major ALB group. Multi-nominal logistic Regression was used to analyze the relationship of pregnancy-related anxiety with autism-like behaviors. Results: Compared with non-ALB group, children whose mother with pregnancy-related anxiety during both trimesters presented significant higher risk on ALB than children whose mother without pregnancy-related anxiety in these two periods (relative risk, RR=2.43, 95% CI: 1.21-4.86, P=0.012), major factors as pregnant women’s IQ and gestational diabetes mellitus, premature delivery and education levels of fosterers on these pregnant women were under control. Our results from the stratified analysis showed: when in the subgroup that mother was the main fosterer of the child, there was an significant increase of risk in children whose mothers with pregnancy-related anxiety during both trimesters (RR=4.22, 95%CI: 1.73-10.32, P=0.002). Conclusion: The association between pregnancy-related anxiety and autism-like behavior was not strong but influenced by the fosterer of the child.

Lien vers le texte intégral (Open Access ou abonnement)