1. Allen JL, Oberdorster G, Morris-Schafer K, Wong C, Klocke C, Sobolewski M, Conrad K, M MP, Cory-Slechta DA. {{Developmental Neurotoxicity of Inhaled Ambient Ultrafine Particle Air Pollution: Parallels with Neuropathological and Behavioral Features of Autism and Other Neurodevelopmental Disorders}}. {Neurotoxicology}. 2015.
Accumulating evidence from both human and animal studies show that brain is a target of air pollution. Multiple epidemiological studies have now linked components of air pollution to diagnosis of autism spectrum disorder (ASD), a linkage with plausibility based on the shared mechanisms of inflammation. Additional plausibility appears to be provided by findings from our studies in mice of exposures from postnatal day (PND) 4-7 and 10-13 (human 3rd trimester equivalent), to concentrated ambient ultrafine (UFP) particles, considered the most reactive component of air pollution, at levels consistent with high traffic areas of major U.S. cities and thus highly relevant to human exposures. These exposures, occurring during a period of marked neuro- and gliogenesis, unexpectedly produced a pattern of developmental neurotoxicity notably similar to multiple hypothesized mechanistic underpinnings of ASD, including its greater impact in males. UFP exposures induced inflammation/microglial activation, reductions in size of the corpus callosum (CC) and associated hypomyelination, aberrant white matter development and/or structural integrity with ventriculomegaly (VM), elevated glutamate and excitatory/inhibitory imbalance, increased amygdala astrocytic activation, and repetitive and impulsive behaviors. Collectively, these findings suggest the human 3rd trimester equivalent as a period of potential vulnerability to neurodevelopmental toxicity to UFP, particularly in males, and point to the possibility that UFP air pollution exposure during periods of rapid neuro- and gliogenesis may be a risk factor not only for ASD, but also for other neurodevelopmental disorders that share features with ASD, such as schizophrenia, attention deficit disorder, and periventricular leukomalacia.
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2. Foster NE, Ouimet T, Tryfon A, Doyle-Thomas K, Anagnostou E, Hyde KL. {{Effects of Age and Attention on Auditory Global-Local Processing in Children with Autism Spectrum Disorder}}. {J Autism Dev Disord}. 2016.
In vision, typically-developing (TD) individuals perceive « global » (whole) before « local » (detailed) features, whereas individuals with autism spectrum disorder (ASD) exhibit a local bias. However, auditory global-local distinctions are less clear in ASD, particularly in terms of age and attention effects. To these aims, here ASD and TD children judged local and global pitch structure in nine-tone melodies. Both groups showed a similar global precedence effect, but ASD children were less sensitive to global interference than TD children at younger ages. There was no effect of attention task. These findings provide novel evidence of developmental differences in auditory perception and may help to refine sensory phenotypes in ASD.
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3. Hens K, Peeters H, Dierickx K. {{Shooting a moving target. Researching autism genes: an interview study with professionals}}. {Eur J Med Genet}. 2015.
BACKGROUND: Given the wide variety of the phenotype, the uncertain genetic origins and the discussions surrounding the status of autism itself, genetic research on autism genes generates specific ethical questions that are not completely analogous to the ethical issues of genetic research in general. METHOD: In order to map ethical issues surrounding research on autism genes, as experienced by professionals in the field of autism, we interviewed 15 Belgian professionals. RESULTS: We found that respondents believed that the heterogeneity of the autism phenotype affects the ethics of research on several levels. It affects issues regarding who to include in research on autism genes, regarding what the aim is of such studies, and how the research is done. CONCLUSIONS: Although genetic research on autism genes is proliferating, a systematic ethical reflection and protocol is missing. With this study we have shown that autism professionals in Belgium express both skepticism and hope with regard to genetic research and raise important points with regard to the effect that the complexity of autism has on research aims and methodology.
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4. Herguner A, Herguner S. {{Association between age at menarche and autistic traits in Turkish university students}}. {Am J Hum Biol}. 2016; 28(1): 44-7.
OBJECTIVES: The androgen theory of autism suggests that masculinizing effect of fetal androgens may play a role in the expression of autism. Recent evidence showed that excessive prenatal androgen exposure might delay age at menarche (AAM). The aim of this study was to investigate the relation between autistic traits and AAM in a sample of nonclinical female university students. METHODS: Autistic traits were measured using the Autism Spectrum Quotient (AQ), and AAM was questioned by retrospective self-reports. The AQ was completed by 436 female university students. RESULTS: There were significant positive correlations between AAM and AQ total and subscales measuring Social Skills, Communication, and Imagination. Subjects with above average autistic traits reported later AAM than subjects with below average autistic traits. CONCLUSION: These findings suggest that there may be a common developmental mechanism between delayed menarche and autistic traits, possibly through elevated levels of prenatal androgens. Am. J. Hum. Biol. 28:44-47, 2016. (c) 2015 Wiley Periodicals, Inc.
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5. Lu J, Kishida K, De Asis Cruz J, Lohrenz T, Deering DT, Beauchamp M, Montague PR. {{Single stimulus fMRI produces a neural individual difference measure for Autism Spectrum Disorder}}. {Clin Psychol Sci}. 2015; 3(3): 422-32.
Functional magnetic resonance imaging typically makes inferences about neural substrates of cognitive phenomena at the group level. We report the use of a single-stimulus BOLD response in the cingulate cortex that differentiates individual children with autism spectrum disorder from matched typically developing control children with sensitivity and specificity of 63.6% and 73.7% respectively. The approach consists of passive viewing of ‘self’ and ‘other’ faces from which an individual difference measure is derived from the BOLD response to the first ‘self’ image only; the method, penalized logistic regression, requires no averaging over stimulus presentations or individuals. These findings show that single-stimulus fMRI responses can be extracted from individual subjects and used profitably as a neural individual difference measure. The result suggests that single-stimulus fMRI can be developed to produce quantitative neural biomarkers for other developmental disorders and may even be useful in the rapid typing of cognition in healthy individuals.
