1. Azad G, Blacher J, Marcoulides GA. {{Mothers of children with developmental disabilities: Stress in early and middle childhood}}. {Res Dev Disabil};2013 (Aug 3);34(10):3449-3459.
Using a sample of 219 families of children with (n=94) and without (n=125) developmental disabilities, this study examined the longitudinal perspectives of maternal stress in early (ages 3-5) and middle childhood (ages 6-13) and its relationship to mothers’ and children’s characteristics. Multivariate latent curve models indicated that maternal stress remained high and stable with minimal individual variation in early childhood, but declined with significant individual variation in middle childhood. Maternal stress at the beginning of middle childhood was associated with earlier maternal stress, as well as children’s behavioral problems and social skills. The trajectory of maternal stress across middle childhood was related to children’s behavioral problems. Implications for interventions are discussed.
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2. Essa MM, Subash S, Braidy N, Al-Adawi S, Lim CK, Manivasagam T, Guillemin GJ. {{Role of NAD(+), Oxidative Stress, and Tryptophan Metabolism in Autism Spectrum Disorders}}. {Int J Tryptophan Res};2013;6(Suppl 1):15-28.
Autism spectrum disorder (ASD) is a pervasive neuro-developmental disorder characterized by impaired social interaction, reduced/absent verbal and non-verbal communication, and repetitive behavior during early childhood. The etiology of this developmental disorder is poorly understood, and no biomarkers have been identified. Identification of novel biochemical markers related to autism would be advantageous for earlier clinical diagnosis and intervention. Studies suggest that oxidative stress-induced mechanisms and reduced antioxidant defense, mitochondrial dysfunction, and impaired energy metabolism (NAD(+), NADH, ATP, pyruvate, and lactate), are major causes of ASD. This review provides renewed insight regarding current autism research related to oxidative stress, mitochondrial dysfunction, and altered tryptophan metabolism in ASD.
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3. Garcia-Villamisar D, Rojahn J. {{Comorbid psychopathology and stress mediate the relationship between autistic traits and repetitive behaviours in adults with autism}}. {J Intellect Disabil Res};2013 (Aug 6)
BACKGROUND: Comorbid psychopathology and stress were considered possible mediators that may explain the relationship between some autistic traits and repetitive behaviours. The current study sought to examine the mediational effects of comorbid psychopathology, executive dysfunctions and stress in the relationship between some autistic traits and repetitive behaviours. METHOD: A battery of questionnaires including measures of autistic traits, repetitive behaviours, stress, executive dysfunctions and comorbid psychopathology were administered to a sample of adults with autism and intellectual disabilities (n = 43). RESULTS: We found that when taken as set dimensions of comorbidity, dysexecutive functioning and stress mediated or explained the effects of autistic symptoms on repetitive behaviour. The total model explained 60% of the variation in repetitive behaviours (R = 0.60; F = 13.64, P < 0.001). The results are discussed in the light of pertinent previous research and their clinical implications, and suggestions for future research are provided. CONCLUSIONS: According to the investigated model, increased levels of comorbid psychopathology and stress explained the relationships between repetitive/restrictive behaviours and autistic traits in adults with autism, while executive functioning did not contribute to that relationship.
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4. Ghaziuddin M, Al-Owain M. {{Autism Spectrum Disorders and Inborn Errors of Metabolism: An Update}}. {Pediatr Neurol};2013 (Aug 3)
BACKGROUND: Autism spectrum disorder is characterized by social communicative deficits with restricted interests occurring in about 1% of the population. Although its exact cause is not known, several factors have been implicated in its etiology, including inborn errors of metabolism. Although relatively uncommon, these disorders frequently occur in countries with high rates of consanguinity and are often associated with behavioral problems, such as hyperactivity and aggression. The aim of this review is to examine the association of autism with these conditions. METHOD: A computer-assisted search was performed to identify the most common inborn errors of metabolism associated with autism. RESULTS: The following disorders were identified: phenylketonuria, glucose-6-phosphatase deficiency, propionic acidemia, adenosine deaminase deficiency, Smith-Lemli-Opitz syndrome and mitochondrial disorders, and the recently described branched chain ketoacid dehydrogenase kinase deficiency. CONCLUSION: The risk of autistic features is increased in children with inborn errors of metabolism, especially in the presence of cognitive and behavioral deficits. We propose that affected children should be screened for autism.
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5. Kern JK, Geier DA, Sykes LK, Geier MR. {{Evidence of neurodegeneration in autism spectrum disorder}}. {Transl Neurodegener};2013 (Aug 8);2(1):17.
Autism spectrum disorder (ASD) is a neurological disorder in which a significant number of children experience a developmental regression characterized by a loss of previously-acquired skills and abilities. Loss of neurological function in ASD, as observed in affected children who have regressed, can be explained as neurodegeneration. Although there is research evidence of neurodegeneration or progressive encephalopathy in ASD, the issue of neurodegeneration in ASD is still under debate. Evidence of neurodegeneration in the brain in ASD includes: (1) neuronal cell loss, (2) activated microglia and astrocytes, (3) proinflammatory cytokines, (4) oxidative stress, and (5) elevated 8-oxo-guanosine levels. The evidence from this review suggests that neurodegeneration underlies the loss of neurological function in children with ASD who have experienced regression and loss of previously acquired skills and abilities, and that research into treatments to address the issue of neurodegeneration in ASD are warranted.
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6. Nilsen RM, Suren P, Gunnes N, Alsaker ER, Bresnahan M, Hirtz D, Hornig M, Lie KK, Lipkin WI, Reichborn-Kjennerud T, Roth C, Schjolberg S, Davey Smith G, Susser E, Vollset SE, Oyen AS, Magnus P, Stoltenberg C. {{Analysis of Self-selection Bias in a Population-based Cohort Study of Autism Spectrum Disorders}}. {Paediatr Perinat Epidemiol};2013 (Jul 25)
BACKGROUND: This study examined potential self-selection bias in a large pregnancy cohort by comparing exposure-outcome associations from the cohort to similar associations obtained from nationwide registry data. The outcome under study was specialist-confirmed diagnosis of autism spectrum disorders (ASDs). METHODS: The cohort sample (n = 89 836) was derived from the population-based prospective Norwegian Mother and Child Cohort Study and its substudy of ASDs, the Autism Birth Cohort (ABC) study. The nationwide registry data were derived from the Medical Birth Registry of Norway (n = 507 856). The children were born in 1999-2007, and seven prenatal and perinatal exposures were selected for analyses. RESULTS: ASDs were reported for 234 (0.26%) children in the cohort and 2072 (0.41%) in the nationwide population. Compared with the nationwide population, the cohort had an under-representation of the youngest women (<25 years), those who had single status, mothers who smoked during pregnancy, and non-users of prenatal folic acid supplements. The ratios of the adjusted odds ratios (ORs) in the cohort over the adjusted ORs in the nationwide population were as follows; primipara pregnancy: 1.39/1.22, prenatal folic acid use: 0.85/0.86, prenatal smoking: 1.20/1.17, preterm birth (<37 weeks): 1.48/1.42, low birthweight (<2500 g): 1.60/1.58, male sex: 4.39/4.59 (unadjusted only); and caesarean section history: 1.03/1.04. CONCLUSIONS: Associations estimated between ASDs and perinatal and prenatal exposures in the cohort are close to those estimated in the nationwide population. Self-selection does not appear to compromise validity of exposure-outcome associations in the ABC study.
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7. Suter B, Treadwell-Deering D, Zoghbi HY, Glaze DG, Neul JL. {{Brief Report: MECP2 Mutations in People Without Rett Syndrome}}. {J Autism Dev Disord};2013 (Aug 7)
Mutations in Methyl-CpG-Binding protein 2 (MECP2) are commonly associated with the neurodevelopmental disorder Rett syndrome (RTT). However, some people with RTT do not have mutations in MECP2, and interestingly there have been people identified with MECP2 mutations that do not have the clinical features of RTT. In this report we present four people with neurodevelopmental abnormalities and clear RTT-disease causing MECP2 mutation but lacking the characteristic clinical features of RTT. One patient’s symptoms suggest an extension of the known spectrum of MECP2 associated phenotypes to include global developmental delay with obsessive compulsive disorder and attention deficit hyperactivity disorder. These results reemphasize that RTT should remain a clinical diagnosis, based on the recent consensus criteria.
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8. Swanson MR, Siller M. {{Brief Report: Broad Autism Phenotype in Adults is Associated with Performance on an Eye-Tracking Measure of Joint Attention}}. {J Autism Dev Disord};2013 (Aug 7)
The current study takes advantage of modern eye-tracking technology and evaluates how individuals allocate their attention when viewing social videos that display an adult model who is gazing at a series of targets that appear and disappear in the four corners of the screen (congruent condition), or gazing elsewhere (incongruent condition). Data demonstrated the feasibility of administrating this experimental paradigm to a diverse sample of healthy adult college students (N = 44). Results revealed that individual differences in gaze allocation were significantly related to a self-report measure evaluating features of the broad autism phenotype, suggesting that individual variation in the broad autism phenotype is related to individual differences in gaze allocation.
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9. Wu CC, Chiang CH. {{The developmental sequence of socialcommunicative skills in young children with autism: A longitudinal study}}. {Autism};2013 (Aug 6)
To explore the different developmental trajectories of social-communicative skills in children with autism and typically developing infants, two longitudinal studies were conducted. In Study 1, we examined the developmental sequence of social-communicative skills in 26 typically developing infants when they were 9 months old and reexamined them when they were 12 and 15 months old. The results indicated a reliable developmental sequence of social-communicative skills in infants with typical development. In Study 2, we explored the emergence sequence of social-communicative skills of 23 children with autism and 23 children with developmental delay between the ages of 2 and 4 years. The results demonstrated that the developmental sequence of social-communicative skills in young children with autism and children with developmental delays was different.
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10. Zand DH, Braddock B, Baig W, Deasy J, Maxim R. {{Role of Pediatricians in Fostering Resilience in Parents of Children with Autism Spectrum Disorders}}. {J Pediatr};2013 (Aug 3)
