1. Ciernia AV, LaSalle J. {{The landscape of DNA methylation amid a perfect storm of autism aetiologies}}. {Nat Rev Neurosci};2016 (May 6)
Increasing evidence points to a complex interplay between genes and the environment in autism spectrum disorder (ASD), including rare de novo mutations in chromatin genes such as methyl-CpG binding protein 2 (MECP2) in Rett syndrome. Epigenetic mechanisms such as DNA methylation act at this interface, reflecting the plasticity in metabolic and neurodevelopmentally regulated gene pathways. Genome-wide studies of gene sequences, gene pathways and DNA methylation are providing valuable mechanistic insights into ASD. The dynamic developmental landscape of DNA methylation is vulnerable to numerous genetic and environmental insults: therefore, understanding pathways that are central to this ‘perfect storm’ will be crucial to improving the diagnosis and treatment of ASD.
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2. Kodak T, Campbell V, Bergmann S, LeBlanc B, Kurtz-Nelson E, Cariveau T, Haq S, Zemantic P, Mahon J. {{Examination of efficacious, efficient, and socially valid error-correction procedures to teach sight words and prepositions to children with autism spectrum disorder}}. {J Appl Behav Anal};2016 (May 6)
Prior research shows that learners have idiosyncratic responses to error-correction procedures during instruction. Thus, assessments that identify error-correction strategies to include in instruction can aid practitioners in selecting individualized, efficacious, and efficient interventions. The current investigation conducted an assessment to compare 5 error-correction procedures that have been evaluated in the extant literature and are common in instructional practice for children with autism spectrum disorder (ASD). Results showed that the assessment identified efficacious and efficient error-correction procedures for all participants, and 1 procedure was efficient for 4 of the 5 participants. To examine the social validity of error-correction procedures, participants selected among efficacious and efficient interventions in a concurrent-chains assessment. We discuss the results in relation to prior research on error-correction procedures and current instructional practices for learners with ASD.
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3. Lecavalier L. {{Autism spectrum disorder clinical trials: One step at a time}}. {Autism};2016 (Feb);20(2):131-133.
4. Neely KA, Mohanty S, Schmitt LM, Wang Z, Sweeney JA, Mosconi MW. {{Motor Memory Deficits Contribute to Motor Impairments in Autism Spectrum Disorder}}. {J Autism Dev Disord};2016 (May 7)
Sensorimotor abnormalities are common in individuals with autism spectrum disorder (ASD); however, the processes underlying these deficits remain unclear. This study examined force production with and without visual feedback to determine if individuals with ASD can utilize internal representations to guide sustained force. Individuals with ASD showed a faster rate of force decay in the absence of visual feedback. Comparison of force output and tests of social and verbal abilities demonstrated a link between motor memory impairment and social and verbal deficits in individuals with ASD. This finding suggests that deficits in storage or retrieval of motor memories contribute to sensorimotor deficits and implicates frontoparietal networks involved in short-term consolidation of action dynamics used to optimize ongoing motor output.
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5. Rizzo SJ. {{Repetitive Behavioral Assessments for Compound Screening in Mouse Models of Autism Spectrum Disorders}}. {Methods Mol Biol};2016;1438:293-310.
Treatments for repetitive behaviors in Autism Spectrum Disorders (ASD) and other neurodevelopmental disorders remain an unmet medical need. Mouse models are highly valuable tools for investigating the underlying pathophysiology, genetics, and neurocircuitry of ASD, and can also be characterized for ASD-related phenotypes including repetitive behaviors and stereotypies. This chapter describes methods that can be employed for the assessment of repetitive behavior phenotypes and the evaluation of the ability of test compounds to attenuate repetitive behaviors in mouse models of ASD.
