1. Atladottir HO, Thorsen P, Ostergaard L, Schendel DE, Lemcke S, Abdallah M, Parner ET. {{Maternal Infection Requiring Hospitalization During Pregnancy and Autism Spectrum Disorders}}. {J Autism Dev Disord} (Apr 23)
Exposure to prenatal infection has been suggested to cause deficiencies in fetal neurodevelopment. In this study we included all children born in Denmark from 1980, through 2005. Diagnoses of autism spectrum disorders (ASDs) and maternal infection were obtained through nationwide registers. Data was analyzed using Cox proportional hazards regression. No association was found between any maternal infection and diagnosis of ASDs in the child when looking at the total period of pregnancy: adjusted hazard ratio = 1.14 (CI: 0.96-1.34). However, admission to hospital due to maternal viral infection in the first trimester and maternal bacterial infection in the second trimester were found to be associated with diagnosis of ASDs in the offspring, adjusted hazard ratio = 2.98 (CI: 1.29-7.15) and adjusted hazard ratio = 1.42 (CI: 1.08-1.87), respectively. Our results support prior hypotheses concerning early prenatal viral infection increasing the risk of ASDs.
2. Charman T. {{Autism Research Comes of (a Young) Age}}. {J Am Acad Child Adolesc Psychiatry} (Mar);49(3):208-209.
3. Kantojarvi K, Onkamo P, Vanhala R, Alen R, Hedman M, Sajantila A, Nieminen-von Wendt T, Jarvela I. {{Analysis of 9p24 and 11p12-13 regions in autism spectrum disorders: rs1340513 in the JMJD2C gene is associated with ASDs in Finnish sample}}. {Psychiatr Genet} (Apr 20)
OBJECTIVE: Autism spectrum disorders (ASD) often show obsessive repetitive symptoms that are characteristic to obsessive-compulsive disorder (OCD). Aberrant glutamate function has been suggested to a risk for both ASDs and OCD. Considering the common metabolic pathway and recent results from association studies both in OCD and ASDs, a question, whether there is common molecular background in ASDs and OCD, was raised. METHODS: Ten single nucleotide polymorphisms (SNPs) at 9p24 and 11p12-p13 containing glutamate transporter genes SLC1A1 and SLC1A2 and their neighboring regions in 175 patients with ASDs and 216 controls of Finnish origin were analyzed using real-time-PCR or direct sequencing. RESULTS: The strongest association was detected with rs1340513 in the JMJD2C gene at 9p24.1 (P=0.007; corrected P=0.011) that is the same SNP associated with infantile autism (P=0.0007) in the autism genome project consortium (2007). No association was detected at 11p12-p13 with ASD. Interestingly, the strongest association in OCD has been found at rs301443 (P=0.000067) residing between SLC1A1 and JMJD2C at 9p24. CONCLUSION: In summary, our results give evidence for a possible common locus for OCD and ASDs at 9p24. We speculate that the area may represent a special candidate region for obsessive repetitive symptoms in ASDs.
4. Main PA, Angley MT, Thomas P, O’Doherty CE, Fenech M. {{Folate and methionine metabolism in autism: a systematic review}}. {Am J Clin Nutr} (Apr 21)
BACKGROUND: Autism is a complex neurodevelopmental disorder that is increasingly being recognized as a public health issue. Recent evidence has emerged that children with autism may have altered folate or methionine metabolism, which suggests the folate-methionine cycle may play a key role in the etiology of autism. OBJECTIVE: The objective was to conduct a systematic review to examine the evidence for the involvement of alterations in folate-methionine metabolism in the etiology of autism. DESIGN: A systematic literature review was conducted of studies reporting data for metabolites, interventions, or genes of the folate-methionine pathway in autism. Eighteen studies met the inclusion criteria, 17 of which provided data on metabolites, 5 on interventions, and 6 on genes and their related polymorphisms. RESULTS: The findings of the review were conflicting. The variance in results can be attributed to heterogeneity between subjects with autism, sampling issues, and the wide range of analytic techniques used. Most genetic studies were inadequately powered to provide more than an indication of likely genetic relations. CONCLUSIONS: The review concluded that further research is required with appropriately standardized and adequately powered study designs before any definitive conclusions can be made about the role for a dysfunctional folate-methionine pathway in the etiology of autism. There is also a need to determine whether functional benefits occur when correcting apparent deficits in folate-methionine metabolism in children with autism.
5. Malisza KL, Clancy C, Shiloff D, Foreman D, Holden J, Jones C, Paulson K, Summers R, Yu CT, Chudley AE. {{Functional Evaluation of Hidden Figures Object Analysis in Children with Autistic Disorder}}. {J Autism Dev Disord} (Apr 22)
Functional magnetic resonance imaging (fMRI) during performance of a hidden figures task (HFT) was used to compare differences in brain function in children diagnosed with autism disorder (AD) compared to children with attention-deficit/hyperactivity disorder (ADHD) and typical controls (TC). Overall greater functional MRI activity was observed in the two control groups compared to children with AD. Laterality differences were also evident, with AD subjects preferentially showing activity in the right medial temporal region while controls tended to activate the left medial temporal cortex. Reduced fMRI activity was observed in the parietal, ventral-temporal and hippocampal regions in the AD group, suggesting differences in the way that children with AD process the HFT.
6. Ozonoff S, Iosif AM, Baguio F, Cook IC, Hill MM, Hutman T, Rogers SJ, Rozga A, Sangha S, Sigman M, Steinfeld MB, Young GS. {{A prospective study of the emergence of early behavioral signs of autism}}. {J Am Acad Child Adolesc Psychiatry} (Mar);49(3):256-266e252.
OBJECTIVE:: To examine prospectively the emergence of behavioral signs of autism in the first years of life in infants at low and high risk for autism. METHOD:: A prospective longitudinal design was used to compare 25 infants later diagnosed with an autism spectrum disorder (ASD) with 25 gender-matched low-risk children later determined to have typical development. Participants were evaluated at 6, 12, 18, 24, and 36 months of age. Frequencies of gaze to faces, social smiles, and directed vocalizations were coded from video and rated by examiners. RESULTS:: The frequency of gaze to faces, shared smiles, and vocalizations to others were highly comparable between groups at 6 months of age, but significantly declining trajectories over time were apparent in the group later diagnosed with ASD. Group differences were significant by 12 months of age on most variables. Although repeated evaluation documented loss of skills in most infants with ASD, most parents did not report a regression in their child’s development. CONCLUSIONS:: These results suggest that behavioral signs of autism are not present at birth, as once suggested by Kanner, but emerge over time through a process of diminishment of key social communication behaviors. More children may present with a regressive course than previously thought, but parent report methods do not capture this phenomenon well. Implications for onset classification systems and clinical screening are also discussed.
7. South M, Dana J, White SE, Crowley MJ. {{Failure is Not an Option: Risk-Taking is Moderated by Anxiety and Also by Cognitive Ability in Children and Adolescents Diagnosed with an Autism Spectrum Disorder}}. {J Autism Dev Disord} (Apr 23)
Understanding hetereogeneity in symptom expression across the autism spectrum disorders (ASD) is a major challenge for identifying causes and effective treatments. In 40 children and adolescents diagnosed with ASD and 37 IQ-and age-matched comparison participants (the TYP group), we found no differences in summary measures on an experimental risk-taking task. However, anxiety and IQ predicted risk-taking only in the ASD group. Risk-taking was correlated with behavioral inhibition in the ASD group and behavioral activation in the TYP group. We suggest that performance on the task was motivated by fear of failure in the ASD group and by sensitivity to reward in the TYP group. Behavioral markers of anxiety and cognitive ability may improve conceptualization of heterogeneity in ASD.
8. Stilp RL, Gernsbacher MA, Schweigert EK, Arneson CL, Goldsmith HH. {{Genetic variance for autism screening items in an unselected sample of toddler-age twins}}. {J Am Acad Child Adolesc Psychiatry} (Mar);49(3):267-276.
OBJECTIVE:: Twin and family studies of autistic traits and of cases diagnosed with autism suggest high heritability; however, the heritability of autistic traits in toddlers has not been investigated. Therefore, this study’s goals were (1) to screen a statewide twin population using items similar to the six critical social and communication items widely used for autism screening in toddlers (Modified Checklist for Autism in Toddlers); (2) to assess the endorsement rates of these items in a general population; and (3) to determine their heritability. METHOD:: Participants composed a statewide, unselected twin population. Screening items were administered to mothers of 1,211 pairs of twins between 2 and 3 years of age. Twin similarity was calculated via concordance rates and tetrachoric and intraclass correlations, and the contribution of genetic and environmental factors was estimated with single-threshold ordinal models. RESULTS:: The population-based twin sample generated endorsement rates on the analogs of the six critical items similar to those reported by the scale’s authors, which they used to determine an autism threshold. Current twin similarity and model-fitting analyses also used this threshold. Casewise concordance rates for monozygotic (43%) and dizygotic (20%) twins suggested moderate heritability of these early autism indicators in the general population. Variance component estimates from model-fitting also suggested moderate heritability of categorical scores. CONCLUSIONS:: Autism screener scores are moderately heritable in 2- to 3-year-old twin children from a population-based twin panel. Inferences about sex differences are limited by the scarcity of females who scored above the threshold on the toddler-age screener.
9. van Haaren F. {{Risperidone and parent training in pervasive developmental disorders}}. {J Am Acad Child Adolesc Psychiatry} (Apr);49(4):406-407.
10. Whitehouse AJ, Hickey M, Stanley FJ, Newnham JP, Pennell CE. {{Brief Report: A Preliminary Study of Fetal Head Circumference Growth in Autism Spectrum Disorder}}. {J Autism Dev Disord} (Apr 23)
Fetal head circumference (HC) growth was examined prospectively in children with autism spectrum disorder (ASD). ASD participants (N = 14) were each matched with four control participants (N = 56) on a range of parameters known to influence fetal growth. HC was measured using ultrasonography at approximately 18 weeks gestation and again at birth using a paper tape-measure. Overall body size was indexed by fetal femur-length and birth length. There was no between-groups difference in head circumference at either time-point. While a small number of children with ASD had disproportionately large head circumference relative to body size at both time-points, the between-groups difference did not reach statistical significance in this small sample. These preliminary findings suggest that further investigation of fetal growth in ASD is warranted.
11. Zinke K, Fries E, Kliegel M, Kirschbaum C, Dettenborn L. {{Children with high-functioning autism show a normal cortisol awakening response (CAR)}}. {Psychoneuroendocrinology} (Apr 19)
Individuals with high-functioning autism spectrum disorders (HFA) show difficulties in the ability to react to change. A recent study suggested that variations in the functioning of the hypothalamus-pituitary-adrenal axis, especially in one of its markers – the cortisol awakening response (CAR) – may be related to those difficulties in adolescents with Asperger’s syndrome. The current study investigated the CAR in a younger sample with diagnoses from the whole autism spectrum: A group of children with HFA (N=15) was compared to a group of typically developing children (N=25). Findings suggest that the frequency of a CAR as well as the increase in cortisol levels from awakening to 30min later were similar between groups, indicating that variations in the CAR in HFA may not be present early in life but only develop later in adolescence or may only occur in some diagnoses from the autism spectrum.
