1. Bitsika V, Sharpley CF. {{Using parent- and self-reports to evaluate eating disturbances in young girls with Autism Spectrum Disorder}}. {Int J Dev Neurosci}. 2017; 65: 91-8.
BACKGROUND: Eating Disturbances (ED) often occur in Autism Spectrum Disorder (ASD) but most previous studies have relied on parent-reported data about males with ASD. Few studies have collected data from younger girls with ASD using self-reports and parents’ reports. AIMS: To compare self-reports and parents’ reports of ED in a sample of 52 young girls with ASD, a standardised scale for ED was revised for use with younger girls with ASD. METHODS: Mothers of 52 girls with ASD aged from 6 to 17 years completed the Swedish Eating Assessment for Autism spectrum disorders (SWEAA) on their daughters; the girls also completed the SWEAA as a self-report. RESULTS: The prevalence of severe ED in the sample was low (about 11%). There were minimal significant differences between mothers’ and daughters’ SWEAA responses across most SWEAA subscales. Deletion of several of the original SWEAA items produced a scale that can be used as a self-report or a carer-report with young girls with ASD. CONCLUSION: The clinical assessment of ED via self- or parent reports is suggested as a pathway to identify girls with ASD who also exhibit ED so that adequate treatment planning can be developed for them.
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2. Bonnet-Brilhault F, Malvy J, Tuller L, Prevost P, Zebib R, Ferre S, Santos CD, Roux S, Houy-Durand E, Magne R, Mofid Y, Latinus M, Wardak C, Aguillon-Hernandez N, Batty M, Gomot M. {{A strategic plan to identify key neurophysiological mechanisms and brain circuits in autism}}. {J Chem Neuroanat}. 2017.
Autism and Autism Spectrum Disorder (ASD) cover a large variety of clinical profiles which share two main dimensions: social and communication impairment and repetitive behaviors or restricted interests, which are present during childhood. There is now no doubt that genetic factors are a major component in the etiology of autism but precise physiopathological pathways are still being investigated. Furthermore, developmental trajectories combined with compensatory mechanisms will lead to various clinical and neurophysiological profiles which together constitute this Autism Spectrum Disorder. To better understand the pathophysiology of autism, comprehension of key neurophysiological mechanisms and brain circuits underlying the different bioclinical profiles is thus crucial. To achieve this goal we propose a strategy which investigates different levels of information processing from sensory perception to complex cognitive processing, taking into account the complexity of the stimulus and whether it is social or non-social in nature. In order to identify different developmental trajectories and to take into account compensatory mechanisms, we further propose that such protocols should be carried out in individuals from childhood to adulthood representing a wide variety of clinical forms.
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3. Church JS, Tijerina PB, Emerson FJ, Coburn MA, Blum JL, Zelikoff JT, Schwartzer JJ. {{Perinatal exposure to concentrated ambient particulates results in autism-like behavioral deficits in adult mice}}. {Neurotoxicology}. 2017.
Exposure to fine ambient particulates (PM2.5) during gestation or neonatally has potent neurotoxic effects. While biological and behavioral data indicate a vulnerability to environmental pollutants across distinct neurodevelopmental windows, the behavioral consequences following exposure across the entire developmental period remain unknown. Moreover, several epidemiological studies support a link between developmental exposure to air pollution and an increased risk of later receiving a diagnosis of autism spectrum disorders (ASD), a neurodevelopmental disorder that persists throughout life. In the current study we sought to determine whether perinatal exposure to PM2.5 would reduce sociability and increase repetitive deficits in mice, two hallmark characteristics of ASD. Pregnant female B6C3F1 mice were exposed daily to concentrated ambient PM2.5 (CAPs) (135.8mug/m(3)) or filtered air (3.1mug/m(3)) throughout gestation followed by additional exposures to both dams and their litters from days 2-10 postpartum. Adult offspring were subsequently assessed for social and repetitive behaviors at 20 weeks of age. Daily perinatal exposure to CAPs significantly decreased sociability in male and female mice as measured by the social approach task; however, reductions in reciprocal social interaction and increased grooming behavior were only present in male offspring exposed to CAPs. These findings demonstrate that exposure to particulate air pollutants throughout early neurodevelopment induces long lasting behavioral deficits in a sex-dependent manner and may be an underlying cause of neurodevelopmental disorders such as ASD.
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4. Di X, Azeez A, Li X, Haque E, Biswal BB. {{Disrupted focal white matter integrity in autism spectrum disorder: A voxel-based meta-analysis of diffusion tensor imaging studies}}. {Prog Neuropsychopharmacol Biol Psychiatry}. 2017.
BACKGROUND: Autism spectrum disorder (ASD) is a mental disorder that has long been considered to result from brain underconnectivity. However, volumetric analysis of structural MRI data has failed to find consistent white matter alterations in patients with ASD. The present study aims to examine whether there are consistent focal white matter alterations as measured by diffusion tensor imaging (DTI) in individuals with ASD compared with typically developing (TD) individuals. METHOD: Coordinate-based meta-analysis was performed on 14 studies that reported fractional anisotropy (FA) alterations between individuals with ASD and TD individuals. These studies have in total 297 subjects with ASD and 302 TD subjects. RESULTS: Activation likelihood estimation (ALE) analysis identified two clusters of white matter regions that showed consistent reduction of FA in individuals with ASD compared with TD individuals: the left splenium of corpus callosum and the right cerebral peduncle. CONCLUSIONS: Consistent focal white matter reductions in ASD could be identified by using FA, highlighting the cerebral peduncle which is usually overlooked in studies focusing on major white matter tracts. These focal reductions in the splenium and the cerebral peduncle may be associated with sensorimotor impairments seen in individuals with ASD.
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5. Martinez LA, Tejada-Simon MV. {{Pharmacological Rescue of Hippocampal Fear Learning Deficits in Fragile X Syndrome}}. {Mol Neurobiol}. 2017.
Fragile X Syndrome (FXS) is the leading cause of autism spectrum disorder and intellectual disability and results from loss of Fragile X mental retardation protein (FMRP). In neurons, FMRP controls the translation of synaptic plasticity proteins that are implicated in learning and memory. FMRP also regulates development- and experience-dependent actin cytoskeleton remodeling within dendritic spines through the small Rho GTPase Rac1. Modulation of Rac1 activity is critical during synaptic plasticity as well as learning and memory. We have previously shown that FXS mouse models exhibit learning and memory deficits as well as hyperactive Rac1 in the hippocampus. To determine whether pharmacological inhibition of Rac1 in FXS improves cognitive impairment, FXS mice were treated with the specific Rac1 inhibitor NSC23766, followed by fear conditioning. Whereas non-cognitive functions were unaffected, hippocampus-related memory improved in FXS mice treated with the Rac1 inhibitor. Furthermore, long-term potentiation in hippocampal slices from FXS mice was increased after incubation with the Rac1 inhibitor. Together, these observations indicate that modulation of Rac1 may provide a novel therapeutic target in the treatment of cognitive impairment in FXS.
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6. Skylark WJ, Baron-Cohen S. {{Initial evidence that non-clinical autistic traits are associated with lower income}}. {Mol Autism}. 2017; 8: 61.
Among non-clinical samples, autistic traits correlate with a range of educational and social outcomes. However, previous work has not investigated the relationship between autistic traits and income, a key determinant of socio-economic status and well-being. In five studies (total N = 2491), we recruited participants without a diagnosis of autism from the general US population via an online platform and administered the short-form Autism Spectrum Quotient (AQ) as well as asked a range of demographic questions. We found a negative association between AQ and household income, which remained robust after controlling for age, gender, education, employment status, ethnicity, and socially desirable responding. The effect was primarily driven by the participant’s own income and was mainly due to the social subscale of the AQ. These results provide initial evidence that income is negatively related to autistic traits among the general population, with potential implications for a range of social, psychological, and health outcomes.
