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Papers of the Week

  • 1) Transl Psychiatry. 2014 Sep 9;4:e440. doi: 10.1038/tp.2014.86.

    Testing the accuracy of an observation-based classifier for rapid detection of autism risk.

    Duda M, Kosmicki JA, Wall DP.
    
    PMID: 25203171  [PubMed - as supplied by publisher]
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  • 2) Encephale. 2014 Sep 4. pii: S0013-7006(14)00200-0. doi: 10.1016/j.encep.2014.08.010. [Epub ahead of print]

    [Autism spectrum disorder and suicidality.]

    [Article in French]
    
    Huguet G(1), Contejean Y(2), Doyen C(2).
    
    Author information: 
    (1)Équipe de psychiatrie de liaison, clinique psychiatrique universitaire, CHRU de
    Tours, boulevard Tonnelé, 37044 Tours cedex 01, France. Electronic address:
    g.huguet@chu-tours.fr.
    (2)8(e) secteur de pédopsychiatrie, centre hospitalier Sainte-Anne, 7, rue Cabanis, 
    75674 Paris cedex 14, France.
    
    INTRODUCTION: Most studies on suicide exclude subjects with autism spectrum
    disorders, yet there is a risk group. The purpose of this article is to present
    the data in the literature regarding the clinical and epidemiological
    characteristics of suicidality in subjects with autism spectrum disorders and to 
    identify the factors that promote the transition to action.
    METHODS: This review was carried out using the data set collected in Medline
    PubMed, items with "autism spectrum disorder", "pervasive developmental
    disorder", "Asperger's syndrome", "suicide", "suicide attempt", and "suicide
    behavior".
    RESULTS: In all subjects from our research on PubMed, 21.3% of subjects with
    autism spectrum disorder reported suicidal ideation, have attempted suicide or
    died by suicide (115 out of 539 subjects) and 7.7% of subjects supported for
    suicidal thoughts or attempted suicide exhibited an autism spectrum disorder (62 
    out of 806 subjects), all ages combined. Suicidal ideation and morbid
    preoccupation are particularly common in adolescents and young adults. Suicide
    attempts are accompanied by a willingness for death and can lead to suicide. They
    are more common in high-functioning autism and Asperger subjects. The methods
    used are often violent and potentially lethal or fatal in two cases published.
    Suicide risk depends on many factors that highlight the vulnerability of these
    subjects, following autistic and developmental symptoms. Vulnerability
    complicating the diagnosis of comorbid depressive and anxiety disorders are major
    factors associated with suicidality. Vulnerability but also directly related to
    suicidality, since the origin of physical and sexual abuse and victimization by
    peers assigning them the role of "scapegoat" are both responsible for acting out.
    CONCLUSION: Given the diversity of factors involved in the risk of suicide in
    this population, this does not validate "a" program of intervention, but the
    intervention of "customized programs". Their implementation should be as early as
    possible in order to treat while the brain has the greatest plasticity. The aim
    is to provide the necessary access to the greatest possible autonomy. Hence,
    including working communication skills and interaction, these subject will have
    independent means of protection, an essential complement to measures to protect
    vulnerable subjects; the vulnerability of direct and indirect suicidality.
    Comorbid diagnoses must take into account the specificities of these patients,
    their difficulties in communicating their mental state, and adapted and
    innovative therapeutic strategies must be offered and validated.
    
    Copyright © 2014 L’Encéphale, Paris. Published by Elsevier Masson SAS. All rights
    reserved.
    
    PMID: 25200592  [PubMed - as supplied by publisher]
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  • 3) Dev Med Child Neurol. 2014 Sep 8. doi: 10.1111/dmcn.12581. [Epub ahead of print]

    The association between congenital anomalies and autism spectrum disorders in a Finnish national birth cohort.

    Timonen-Soivio L(1), Vanhala R, Malm H, Leivonen S, Jokiranta E,
    Hinkka-Yli-Salomäki S, Gissler M, Brown AS, Sourander A.
    
    Author information: 
    (1)Department of Child Psychiatry, Turku University and Turku University Central
    Hospital, Turku, Finland.
    
    AIM: The first aim of this study was to evaluate the association between
    different subgroups of autism spectrum disorders (ASDs) (childhood autism,
    Asperger syndrome, and pervasive developmental disorder/pervasive developmental
    disorder - not otherwise specified [PDD/PDD-NOS]) and congenital anomalies.
    Second, we assessed the association among intellectually disabled children with
    ASDs in the subgroups of childhood autism and PDD/PDD-NOS.
    METHOD: Nationwide population-based register data for children with a diagnosis
    of ASD (n=4449; 3548 males, 901 females) were collected during years 1987-2000
    from the Finnish Hospital Discharge Register. Data on congenital anomalies were
    derived from the National Register of Congenital Malformations. Conditional
    logistic regression models were used as a statistical method. The association
    between ASD subgroups and congenital anomalies was stratified by the presence or 
    absence of intellectual disability.
    RESULTS: Congenital anomalies occurred more frequently in all subgroups of ASD
    than in comparison participants (adjusted odds ratio [OR] for major congenital
    anomalies 1.8, 95% confidence interval [CI] 1.5-2.2, p<0.001). The association
    between congenital anomalies and childhood autism (OR 2.4, 95% CI 1.6-3.6,
    p<0.001) and between congenital anomalies and PDD/PDD-NOS (OR 3.7, 95% CI
    2.4-5.7, p<0.001) among children with an intellectual disability was strong but
    remained significant also without intellectual disability (childhood autism: OR
    1.7, 95% CI 1.3-2.3, p<0.001; PDD/PDD-NOS: OR 2.3, 95% CI 1.9-2.8, p<0.001).
    INTERPRETATION: The results suggest a significant association between ASDs and
    congenital anomalies regardless of the ASD subgroup. The association between
    childhood autism and PDD/PDD-NOS and congenital anomalies is stronger among
    children with intellectual disability is stronger than among those without
    intellectual disability. These results may have relevance in examining early risk
    factors in autism during fetal neurodevelopment.
    
    © 2014 Mac Keith Press.
    
    PMID: 25200584  [PubMed - as supplied by publisher]
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  • 4) Curr Probl Pediatr Adolesc Health Care. 2014 Sep 4. pii: S1538-5442(14)00074-1. doi: 10.1016/j.cppeds.2014.06.001. [Epub ahead of print]

    Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence.

    Kalkbrenner AE(1), Schmidt RJ(2), Penlesky AC(1).
    
    Author information: 
    (1)Zilber School of Public Health, University of Wisconsin-Milwaukee, Milwaukee, WI.
    (2)Department of Public Health Sciences, University of California Davis School of
    Medicine, Davis, CA; Medical Investigation of Neurodevelopmental Disorders (MIND)
    Institute, University of California Davis, Sacramento, CA.
    
    In the past decade, the number of epidemiological publications addressing
    environmental chemical exposures and autism has grown tremendously. These studies
    are important because it is now understood that environmental factors play a
    larger role in causing autism than previously thought and because they address
    modifiable risk factors that may open up avenues for the primary prevention of
    the disability associated with autism. In this review, we covered studies of
    autism and estimates of exposure to tobacco, air pollutants, volatile organic
    compounds and solvents, metals (from air, occupation, diet, dental amalgams, and 
    thimerosal-containing vaccines), pesticides, and organic endocrine-disrupting
    compounds such as flame retardants, non-stick chemicals, phthalates, and
    bisphenol A. We included studies that had individual-level data on autism,
    exposure measures pertaining to pregnancy or the 1st year of life, valid
    comparison groups, control for confounders, and adequate sample sizes. Despite
    the inherent error in the measurement of many of these environmental exposures,
    which is likely to attenuate observed associations, some environmental exposures 
    showed associations with autism, especially traffic-related air pollutants, some 
    metals, and several pesticides, with suggestive trends for some volatile organic 
    compounds (e.g., methylene chloride, trichloroethylene, and styrene) and
    phthalates. Whether any of these play a causal role requires further study. Given
    the limited scope of these publications, other environmental chemicals cannot be 
    ruled out, but have not yet been adequately studied. Future research that
    addresses these and additional environmental chemicals, including their most
    common routes of exposures, with accurate exposure measurement pertaining to
    several developmental windows, is essential to guide efforts for the prevention
    of the neurodevelopmental damage that manifests in autism symptoms.
    
    Copyright © 2014 Mosby, Inc. All rights reserved.
    
    PMID: 25199954  [PubMed - as supplied by publisher]
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  • 5) Mol Psychiatry. 2014 Sep 9. doi: 10.1038/mp.2014.98. [Epub ahead of print]

    Clustering autism: using neuroanatomical differences in 26 mouse models to gain insight into the heterogeneity.

    Ellegood J(1), Anagnostou E(2), Babineau BA(3), Crawley JN(4), Lin L(5),
    Genestine M(5), DiCicco-Bloom E(5), Lai JK(6), Foster JA(6), Peñagarikano O(7),
    Geschwind DH(7), Pacey LK(8), Hampson DR(8), Laliberté CL(1), Mills AA(9), Tam
    E(10), Osborne LR(10), Kouser M(11), Espinosa-Becerra F(11), Xuan Z(11), Powell
    CM(11), Raznahan A(12), Robins DM(13), Nakai N(14), Nakatani J(14), Takumi T(14),
    van Eede MC(1), Kerr TM(15), Muller C(15), Blakely RD(15), Veenstra-VanderWeele
    J(15), Henkelman RM(16), Lerch JP(16).
    
    Author information: 
    (1)Mouse Imaging Centre, Hospital for Sick Children, Toronto, ON, Canada.
    (2)Holland Bloorview Kids Rehabilitation Hospital, Toronto, ON, Canada.
    (3)Laboratory of Behavioral Neurosciences, National Institute of Mental Health,
    Bethesda, MD, USA.
    (4)1] Laboratory of Behavioral Neurosciences, National Institute of Mental Health,
    Bethesda, MD, USA [2] Department of Psychiatry and Behavioral Sciences, MIND
    Institute, University of California Davis School of Medicine, Sacramento, CA,
    USA.
    (5)Department of Neurosciences and Cell Biology, UMDNJ-Robert Wood Johnson Medical
    School, Piscataway, NJ, USA.
    (6)The Brain-Body Institute, McMaster University, Hamilton, ON, Canada.
    (7)Semel Institute for Neuroscience and Human Behavior, David Geffen School of
    Medicine, UCLA, Los Angeles, CA, USA.
    (8)Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, ON, Canada.
    (9)Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA.
    (10)Departments of Medicine and Molecular Genetics, University of Toronto, Toronto,
    ON, Canada.
    (11)Departments of Neurology and Neurotherapeutics, Psychiatry, University of Texas
    Southwestern Medical Center, Dallas, TX, USA.
    (12)Child Psychiatry Branch, National Institutes of Mental Health, Bethesda, MD, USA.
    (13)Department of Human Genetics, University of Michigan Medical School, Ann Arbor,
    MI, USA.
    (14)Department of Mental Biology, RIKEN Brain Science Institute, Wako, Japan.
    (15)Department of Pharmacology, Vanderbilt Kennedy Center, Vanderbilt Brain
    Institute, Nashville, TN, USA.
    (16)1] Mouse Imaging Centre, Hospital for Sick Children, Toronto, ON, Canada [2]
    Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada.
    
    Autism is a heritable disorder, with over 250 associated genes identified to
    date, yet no single gene accounts for >1-2% of cases. The clinical presentation, 
    behavioural symptoms, imaging and histopathology findings are strikingly
    heterogeneous. A more complete understanding of autism can be obtained by
    examining multiple genetic or behavioural mouse models of autism using magnetic
    resonance imaging (MRI)-based neuroanatomical phenotyping. Twenty-six different
    mouse models were examined and the consistently found abnormal brain regions
    across models were parieto-temporal lobe, cerebellar cortex, frontal lobe,
    hypothalamus and striatum. These models separated into three distinct clusters,
    two of which can be linked to the under and over-connectivity found in autism.
    These clusters also identified previously unknown connections between Nrxn1α, En2
    and Fmr1; Nlgn3, BTBR and Slc6A4; and also between X monosomy and Mecp2. With no 
    single treatment for autism found, clustering autism using neuroanatomy and
    identifying these strong connections may prove to be a crucial step in predicting
    treatment response.Molecular Psychiatry advance online publication, 9 September
    2014; doi:10.1038/mp.2014.98.
    
    PMID: 25199916  [PubMed - as supplied by publisher]
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  • 6) Milbank Q. 2014 Sep;92(3):475-508. doi: 10.1111/1468-0009.12075.

    Power and persuasion in the vaccine debates: an analysis of political efforts and outcomes in the United States, 1998-2012.

    Lillvis DF(1), Kirkland A, Frick A.
    
    Author information: 
    (1)University of Michigan; School of Public Health, University of Michigan.
    
    Policy Points: From 2011 to 2013, immunization proponents won significant
    legislative victories that tightened philosophical exemptions in Washington,
    Oregon, and California. Highlighting data on the high rates of unvaccinated
    children and subsequent, preventable infectious disease outbreaks has proven to
    be quite compelling to state lawmakers, especially when combined with physician
    expert testimony. Even vigorous protest from vaccine-critical organizations
    failed to defeat recent legislative wins when other political conditions were
    favorable.  Our research suggests that immunization proponents have not been as
    active as they could be, and that much of the energy in pressing for new policies
    over the past 15 years has been on the vaccine-critical side of the
    aisle. CONTEXT: This article examines trends in state-level childhood vaccine
    policies in the United States from 1998 to 2012 and explains the trajectories for
    both vaccine-critical and proimmunization legislative efforts. Successful
    mobilization by vaccine critics during the height of the autism and thimerosal
    scares (roughly 1998 to 2003) yielded a few state-level expansions for the most
    permissive type of exemption from vaccine mandates for public school attendance, 
    those based on personal beliefs. Vaccine-critical positions, however, have
    largely become discredited. How has vaccine critics' ability to advance preferred
    policies and prevent the passage of unfavorable legislation changed over time?
    METHODS: We created a unique data set of childhood vaccine bills (n = 636),
    introduced from 1998 to 2012 across the 50 state legislatures, and coded them by 
    type of effort (exemption, mandate, mercury ban, and information policies) and
    outcome. We then mapped out the trends in vaccine policies over time. In order to
    contextualize the trends we identified, we also reviewed numerous primary sources
    and conducted interviews with stakeholders.
    FINDINGS: In general, we found that vaccine critics' legislative success has
    begun to wane. In only 20 bills in our data set were vaccine critics able to
    change policy in their preferred direction via the legislative process. Only 5 of
    those wins were significant (such as obtaining a new philosophical exemption to
    vaccine mandates), and the last of these was in 2007. Critics were more
    successful at preventing passage of proimmunization legislation, such as mandates
    for the human papillomavirus (HPV) vaccine.
    CONCLUSIONS: Recent legislation in California, Oregon, and Washington that
    tightened philosophical exemptions by means of informational requirements
    suggests that vaccine politics may be entering another phase, one in which
    immunization supporters may be able to counter increasing opt-out rates,
    particularly in states with recent outbreaks and politicians favoring
    science-based policies.
    
    © 2014 Milbank Memorial Fund.
    
    PMID: 25199897  [PubMed - in process]
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  • 7) J Child Adolesc Psychopharmacol. 2014 Sep 8. [Epub ahead of print]

    Low Rates of Depressed Mood and Depression Diagnoses in a Clinic Review of Children and Adolescents with Autistic Disorder.

    Henry CA(1), Nowinski L, Koesterer K, Ferrone C, Spybrook J, Bauman M.
    
    Author information: 
    (1)1 Department of Psychiatry, Massachusetts General Hospital , Boston,
    Massachusetts.
    
    Abstract Objectives: The purpose of this study was to investigate the prevalence 
    of depression diagnoses and related clinical data in an outpatient sample of
    youth with autistic disorder. Methods: Records of 123 psychiatrically referred
    children and adolescents with a Diagnostic and Statistical Manual of Mental
    Disorders, 4th ed., Text Revision (DSM-IV-TR) diagnosis of autistic disorder were
    examined. Mood disorder diagnoses and chief complaints along with family mood
    disorder history were the primary variables analyzed. Results: Four subjects (3%)
    presented with depressed mood. Irritability complaints were frequent (n=78, 63%).
    Six subjects (5%) received a mood disorder diagnosis; all with mood disorder, not
    otherwise specified. No subjects received a depressive disorder diagnosis. Family
    history of mood disorders was common. Conclusions: Findings raise questions about
    the appropriate characterization and potential misdiagnoses of depression in
    youth with autistic disorder.
    
    PMID: 25198799  [PubMed - as supplied by publisher]
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  • 8) Nat Commun. 2014 Sep 8;5:4692. doi: 10.1038/ncomms5692.

    Loss of Wdfy3 in mice alters cerebral cortical neurogenesis reflecting aspects of the autism pathology.

    Orosco LA(1), Ross AP(1), Cates SL(1), Scott SE(1), Wu D(2), Sohn J(3), Pleasure 
    D(4), Pleasure SJ(5), Adamopoulos IE(2), Zarbalis KS(1).
    
    Author information: 
    (1)1] Department of Pathology and Laboratory Medicine, University of California at
    Davis, Sacramento, California 95817, USA [2] Institute for Pediatric Regenerative
    Medicine, Shriners Hospitals for Children, Northern California, 2425 Stockton
    Boulevard, Sacramento, California 95817, USA.
    (2)1] Institute for Pediatric Regenerative Medicine, Shriners Hospitals for
    Children, Northern California, 2425 Stockton Boulevard, Sacramento, California
    95817, USA [2] Department of Internal Medicine, Division of Rheumatology, Allergy
    and Clinical Immunology, University of California, Davis, California 95616, USA.
    (3)Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children,
    Northern California, 2425 Stockton Boulevard, Sacramento, California 95817, USA.
    (4)1] Institute for Pediatric Regenerative Medicine, Shriners Hospitals for
    Children, Northern California, 2425 Stockton Boulevard, Sacramento, California
    95817, USA [2] Departments of Neurology and Pediatrics, University of California 
    at Davis, Sacramento, California 95817, USA.
    (5)Department of Neurology, Programs in Neuroscience, Developmental and Stem Cell
    Biology, UCSF Institute for Regeneration Medicine, University of California at
    San Francisco, Sandler Neurosciences Center, Box 3206, 675 Nelson Rising Lane,
    Room 214, San Francisco, California 94158, USA.
    
    Autism spectrum disorders (ASDs) are complex and heterogeneous developmental
    disabilities affecting an ever-increasing number of children worldwide. The
    diverse manifestations and complex, largely genetic aetiology of ASDs pose a
    major challenge to the identification of unifying neuropathological features.
    Here we describe the neurodevelopmental defects in mice that carry deleterious
    alleles of the Wdfy3 gene, recently recognized as causative in ASDs. Loss of
    Wdfy3 leads to a regionally enlarged cerebral cortex resembling early brain
    overgrowth described in many children on the autism spectrum. In addition,
    affected mouse mutants display migration defects of cortical projection neurons, 
    a recognized cause of epilepsy, which is significantly comorbid with autism. Our 
    analysis of affected mouse mutants defines an important role for Wdfy3 in
    regulating neural progenitor divisions and neural migration in the developing
    brain. Furthermore, Wdfy3 is essential for cerebral expansion and functional
    organization while its loss-of-function results in pathological changes
    characteristic of ASDs.
    
    PMID: 25198012  [PubMed - as supplied by publisher]
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  • 9) MMWR Surveill Summ. 2014 Sep 12;63:27-35.

    Screening for Developmental Delays Among Young Children --- National Survey of Children's Health, United States, 2007.

    Rice CE, Naarden Braun KV, Kogan MD, Smith C, Kavanagh L, Strickland B, Blumberg 
    SJ.
    
    Early childhood development typically follows a trajectory of achieving physical,
    cognitive, communication, social-emotional, and self-help milestones within a
    specified age range. Although most children reach these milestones within a
    similar range, others exhibit mild to severe developmental delays that indicate
    potential developmental disabilities. Developmental disabilities are a group of
    conditions caused by an impairment in one or more developmental domains (e.g.,
    physical, learning, communication, behavior, or self-help). Developmental
    disabilities can become evident during the prenatal period through age 22 years, 
    affect day-to-day functioning, and usually are lifelong. Approximately 15% of
    children aged 3-17 years in 2008 were estimated to have developmental
    disabilities of varying severity, such as language or learning disorders,
    intellectual disabilities, cerebral palsy, seizures, hearing loss, blindness,
    autism spectrum disorder (ASD), or other developmental delays.
    
    PMID: 25208255  [PubMed - as supplied by publisher]
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  • 10) J Dev Behav Pediatr. 2014 Sep 9. [Epub ahead of print]

    Age at First Autism Spectrum Disorder Diagnosis: The Role of Birth Cohort, Demographic Factors, and Clinical Features.

    Mazurek MO(1), Handen BL, Wodka EL, Nowinski L, Butter E, Engelhardt CR.
    
    Author information: 
    (1)*Department of Health Psychology and Thompson Center for Autism and
    Neurodevelopmental Disorders, University of Missouri, Columbia, MO; †Department
    of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA;
    ‡Department of Psychiatry and Behavioral Sciences, Johns Hopkins University
    School of Medicine and Center for Autism and Related Disorders, Kennedy Krieger
    Institute, Baltimore, MD; §Lurie Center for Autism, MassGeneral Hospital for
    Children, and Harvard Medical School, Boston, MA; ‖Departments of Pediatrics and 
    Psychology, Nationwide Children's Hospital, Ohio State University, Columbus, OH.
    
    OBJECTIVE:: This study sought to identify factors that may be associated with
    delays in autism spectrum disorder (ASD) diagnosis, including birth cohort,
    sociodemographic characteristics, and clinical features.
    METHODS:: Participants included 1716 children and adolescents with ASD enrolled
    in the Autism Speaks Autism Treatment Network (AS-ATN) between the years 2008 and
    2011. Data were collected at enrollment using AS-ATN parent- and clinician-report
    forms and standardized measures of I.Q., ASD symptoms, adaptive function, and
    psychiatric symptoms.
    RESULTS:: Age at first ASD diagnosis was positively correlated with current age, 
    suggesting a birth cohort effect. Sociodemographic and clinical features were
    also associated with age at diagnosis, even after controlling for current age.
    Hierarchical linear regression results showed that older current age, lower
    socioeconomic status (SES), higher I.Q. score, and lower levels of autism
    symptoms were associated with later age at initial diagnosis. There was also a
    significant interaction between current age and I.Q., with higher functioning
    children being diagnosed at younger ages than in previous years.
    CONCLUSIONS:: Early diagnosis of ASD is critically important for improving access
    to interventions; however, many children experience diagnostic delays. In this
    sample, children from the most recent birth cohorts were diagnosed earlier,
    suggesting that early signs of ASD are being increasingly recognized. However,
    socioeconomic barriers to diagnosis still seem to exist. Children with less
    severe ASD symptoms and with higher I.Q. are also diagnosed at later ages.
    Efforts are still needed to reduce diagnostic disparities for families of low SES
    and to improve early recognition of more subtle symptoms.
    
    PMID: 25211371  [PubMed - as supplied by publisher]
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  • 11) J Clin Child Adolesc Psychol. 2014 September-October;43(5):828-843.

    Future Directions for Research in Autism Spectrum Disorders.

    Damiano CR(1), Mazefsky CA, White SW, Dichter GS.
    
    Author information: 
    (1)a Department of Psychology and Carolina Institute for Developmental Disabilities 
    , University of North Carolina at Chapel Hill.
    
    This article suggests future directions for research aimed at improving our
    understanding of the etiology and pathophysiology of autism spectrum disorder
    (ASD) as well as pharmacologic and psychosocial interventions for ASD across the 
    lifespan. The past few years have witnessed unprecedented transformations in the 
    understanding of ASD neurobiology, genetics, early identification, and early
    intervention. However, recent increases in ASD prevalence estimates highlight the
    urgent need for continued efforts to translate novel ASD discoveries into
    effective interventions for all individuals with ASD. In this article we
    highlight promising areas for ongoing and new research expected to quicken the
    pace of scientific discovery and ultimately the translation of research findings 
    into accessible and empirically supported interventions for those with ASD. We
    highlight emerging research in the following domains as particularly promising
    and pressing: (a) preclinical models, (b) experimental therapeutics, (c) early
    identification and intervention, (d) psychiatric comorbidities and the Research
    Domain Criteria initiative, (e) ecological momentary assessment, (f)
    neurotechnologies, and (g) the needs of adults with ASD. Increased research
    emphasis in these areas has the potential to hasten the translation of knowledge 
    on the etiological mechanisms of ASD to psychosocial and biological interventions
    to reduce the burden of ASD on affected individuals and their families.
    
    PMID: 25216048  [PubMed - as supplied by publisher]
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  • 12) J Autism Dev Disord. 2014 Sep 12. [Epub ahead of print]

    Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants.

    Rogers SJ(1), Vismara L, Wagner AL, McCormick C, Young G, Ozonoff S.
    
    Author information: 
    (1)MIND Institute, University of California, Davis, Sacramento, CA, USA,
    sally.rogers@ucdmc.ucdavis.edu.
    
    The goal of early autism screening is earlier treatment. We pilot-tested a
    12-week, low-intensity treatment with seven symptomatic infants ages 7-15 months.
    Parents mastered the intervention and maintained skills after treatment ended.
    Four comparison groups were matched from a study of infant siblings. The treated 
    group of infants was significantly more symptomatic than most of the comparison
    groups at 9 months of age but was significantly less symptomatic than the two
    most affected groups between 18 and 36 months. At 36 months, the treated group
    had much lower rates of both ASD and DQs under 70 than a similarly symptomatic
    group who did not enroll in the treatment study. It appears feasible to identify 
    and enroll symptomatic infants in parent-implemented intervention before
    12 months, and the pilot study outcomes are promising, but testing the
    treatment's efficacy awaits a randomized trial.
    
    PMID: 25212413  [PubMed - as supplied by publisher]
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  • 13) Autism. 2014 Sep 11. pii: 1362361314548731. [Epub ahead of print]

    The role of anger rumination and autism spectrum disorder-linked perseveration in the experience of aggression in the general population.

    Pugliese CE(1), Fritz MS(2), White SW(3).
    
    Author information: 
    (1)Virginia Tech, Virginia, USA Children's National Medical Center, Maryland, USA
    CPuglies@ChildrensNational.org.
    (2)University of Nebraska-Lincoln, Nebraska, USA.
    (3)Virginia Tech, Virginia, USA.
    
    This study (a) examined the role of anger rumination as a mediator of the
    relation between social anxiety and the experience of anger, hostility, and
    aggression, in the general population, and (b) evaluated the degree to which the 
    presence of autism spectrum disorder characteristics moderates the indirect
    influence of anger rumination. We then explored whether social cognition and
    perseveration characteristic of autism spectrum disorder uniquely accounted for
    the predicted moderation. In this survey study of young adults (n = 948), anger
    rumination mediated the relation between social anxiety and hostility, as well as
    verbal and physical aggression, as predicted. Greater autism spectrum disorder
    characteristics augmented the effect of social anxiety on hostility and physical 
    aggression by increasing the effect of anger rumination, but not by increasing
    the effect of social anxiety on anger rumination. Implications for developing
    treatment approaches that target hostility and aggression among young adults who 
    may not be formally diagnosed but have characteristics of autism spectrum
    disorder are discussed.
    
    © The Author(s) 2014.
    
    PMID: 25212211  [PubMed - as supplied by publisher]
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  • 14) Gen Hosp Psychiatry. 2014 Aug 16. pii: S0163-8343(14)00208-4. doi: 10.1016/j.genhosppsych.2014.08.004. [Epub ahead of print]

    Autism spectrum disorder among first-visit depressed adult patients: diagnostic clues from backgrounds and past history.

    Takara K(1), Kondo T(2).
    
    Author information: 
    (1)Department of Neuropsychiatry, Graduate School of Medicine, University of the
    Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan. Electronic address:
    takarakiyo1018@gmail.com.
    (2)Department of Neuropsychiatry, Graduate School of Medicine, University of the
    Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan.
    
    OBJECTIVE: The present study aimed to extract discriminating indicators for
    diagnosis of autism spectrum disorder (ASD) from personal backgrounds and past
    history among depressed adult outpatients.
    METHODS: Subjects were 430 depressed adults, consisting of patients with ASD
    (n=70) and those without ASD (n=360). Group comparison and discriminant analysis 
    was conducted with regard to backgrounds (age, gender, education, marriage,
    living alone, physical diseases and family history of mood disorders) and past
    history (school non-attendance, bullied experience, psychotic-like experiences,
    conduct problems, suicide-related behaviors and interpersonal friction).
    RESULTS: Six discriminating indicators (interpersonal friction, bullied
    experience, psychotic-like experiences, age under 32 years, school non-attendance
    and university educational level) were identified by stepwise discriminant
    analysis (P<.001). Absence of the first 4 indicators almost excluded ASD
    diagnosis with the highest negative predictive value (98%) and the least negative
    likelihood ratio (0.11) whereas one or more out of these 4 indicators showed low 
    positive predictive value (32%) despite high sensitivity (93%).
    CONCLUSIONS: The abovementioned 4 indicators may be useful clues to cover
    possible ASD subjects among depressed adults although further detailed ASD
    focused diagnostic procedure is absolutely necessary to specify true ASD
    subjects. Meanwhile, absence of these 4 indicators is probably helpful to rule
    out ASD diagnosis.
    
    Copyright © 2014. Published by Elsevier Inc.
    
    PMID: 25217491  [PubMed - as supplied by publisher]
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  • 15) J Autism Dev Disord. 2014 Sep 13. [Epub ahead of print]

    Does Gender Influence Core Deficits in ASD? An Investigation into Social-Communication and Play of Girls and Boys with ASD.

    Harrop C(1), Shire S, Gulsrud A, Chang YC, Ishijima E, Lawton K, Kasari C.
    
    Author information: 
    (1)Center for Autism Research and Treatment, Semel Institute for Neuroscience and
    Human Behavior, University of California Los Angeles, 760 Westwood Plaza, Los
    Angeles, CA, 90095, USA, charrop@mednet.ucla.edu.
    
    Due to the predominance of boys diagnosed with autism spectrum disorders (ASD),
    girls are rarely studied independently. Research specifically focusing on play
    and social-communication in girls with ASD is extremely varied. We were
    interested in whether girls with ASD demonstrated equivalent social-communication
    and play skills in early childhood relative to boys, using two measures focused
    on the specific quantification of these variables. We also examined whether the
    associations between developmental variables and social-communication and play
    differed by gender. Forty girls with ASD were individually matched to 40 boys
    based on ASD severity. Our results suggest that girls and boys were more similar 
    than different, however they also raise questions about the potential
    differential associations between development and requesting ability in girls and
    boys with ASD.
    
    PMID: 25217088  [PubMed - as supplied by publisher]
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  • 16) Neuropsychologia. 2014 Sep 8. pii: S0028-3932(14)00307-8. doi: 10.1016/j.neuropsychologia.2014.09.002. [Epub ahead of print]

    Autism spectrum disorder, but not amygdala lesions, impairs social attention in Visual search.

    Wang S(1), Xu J(2), Jiang M(2), Zhao Q(2), Hurlemann R(3), Adolphs R(4).
    
    Author information: 
    (1)Computation and Neural Systems, California Institute of Technology, Pasadena, CA 
    91125, USA. Electronic address: wangshuo45@gmail.com.
    (2)Department of Electrical and Computer Engineering, National University of
    Singapore, 117583 Singapore.
    (3)Department of Psychiatry, University of Bonn, 53105 Bonn, Germany.
    (4)Computation and Neural Systems, California Institute of Technology, Pasadena, CA 
    91125, USA; Humanities and Social Sciences, California Institute of Technology,
    Pasadena, CA 91125, USA.
    
    People with autism spectrum disorders (ASD) have pervasive impairments in social 
    interactions, a diagnostic component that may have its roots in atypical social
    motivation and attention. One of the brain structures implicated in the social
    abnormalities seen in ASD is the amygdala. To further characterize the impairment
    of people with ASD in social attention, and to explore the possible role of the
    amygdala, we employed a series of visual search tasks with both social (faces and
    people with different postures, emotions, ages, and genders) and non-social
    stimuli (e.g., electronics, food, utensils). We first conducted trial-wise
    analyses of fixation properties and elucidated visual search mechanisms. We found
    that an attentional mechanism of initial orientation could explain the detection 
    advantage of non-social targets. We then zoomed into fixation-wise analyses. We
    defined target-relevant effects as the difference in the percentage of fixations 
    that fell on target-congruent vs. target-incongruent items in the array. In
    Experiment 1, we tested 8 high-functioning adults with ASD, 3 adults with focal
    bilateral amygdala lesions, and 19 controls. Controls rapidly oriented to
    target-congruent items and showed a strong and sustained preference for fixating 
    them. Strikingly, people with ASD oriented significantly less and more slowly to 
    target-congruent items, an attentional deficit especially with social targets. By
    contrast, patients with amygdala lesions performed indistinguishably from
    controls. In Experiment 2, we recruited a different sample of 13 people with ASD 
    and 8 healthy controls, and tested them on the same search arrays but with all
    array items equalized for low-level saliency. The results replicated those of
    Experiment 1. In Experiment 3, we recruited 13 people with ASD, 8 healthy
    controls, 3 amygdala lesion patients and another group of 11 controls and tested 
    them on a simpler array. Here our group effect for ASD strongly diminished and
    all four subject groups showed similar target-relevant effects. These findings
    argue for an attentional deficit in ASD that is disproportionate for social
    stimuli, cannot be explained by low-level visual properties of the stimuli, and
    is more severe with high-load top-down task demands. Furthermore, this deficit
    appears to be independent of the amygdala, and not evident from general social
    bias independent of the target-directed search.
    
    Copyright © 2014. Published by Elsevier Ltd.
    
    PMID: 25218953  [PubMed - as supplied by publisher]
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  • 17) Brain Behav Immun. 2014 Sep 10. pii: S0889-1591(14)00452-8. doi: 10.1016/j.bbi.2014.09.001. [Epub ahead of print]

    Maternal hospitalization with infection during pregnancy and risk of autism spectrum disorders.

    Lee BK(1), Magnusson C(2), Gardner RM(3), Blomström S(2), Newschaffer CJ(4),
    Burstyn I(5), Karlsson H(6), Dalman C(2).
    
    Author information: 
    (1)Department of Epidemiology and Biostatistics, Drexel University School of Public 
    Health, Philadelphia, PA, USA; A.J. Drexel Autism Institute, Philadelphia, PA,
    USA. Electronic address: bklee@drexel.edu.
    (2)Division of Public Health Epidemiology, Department of Public Health Sciences,
    Karolinska Institutet, Stockholm, Sweden.
    (3)Division of Public Health Epidemiology, Department of Public Health Sciences,
    Karolinska Institutet, Stockholm, Sweden; Department of Neuroscience, Karolinska 
    Institutet, Stockholm, Sweden.
    (4)Department of Epidemiology and Biostatistics, Drexel University School of Public 
    Health, Philadelphia, PA, USA; A.J. Drexel Autism Institute, Philadelphia, PA,
    USA.
    (5)A.J. Drexel Autism Institute, Philadelphia, PA, USA; Department of Environmental 
    and Occupational Health, Drexel University School of Public Health, Philadelphia,
    PA, USA.
    (6)Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    
    Animal models indicate that maternal infection during pregnancy can result in
    behavioral abnormalities and neuropathologies in offspring. We examined the
    association between maternal inpatient diagnosis with infection during pregnancy 
    and risk of ASD in a Swedish nationwide register-based birth cohort born
    1984-2007 with follow-up through 2011. In total, the sample consisted of
    2,371,403 persons with 24,414 ASD cases. Infection during pregnancy was defined
    from ICD codes. In the sample, 903 mothers of ASD cases (3.7%) had an inpatient
    diagnosis of infection during pregnancy. Logistic regression models adjusted for 
    a number of covariates yielded odds ratios indicating approximately a 30%
    increase in ASD risk associated with any inpatient diagnosis of infection. Timing
    of infection did not appear to influence risk in the total Swedish population,
    since elevated risk of ASD was associated with infection in all trimesters. In a 
    subsample analysis, infections were associated with greater risk of ASD with
    intellectual disability than for ASD without intellectual disability. The present
    study adds to the growing body of evidence, encompassing both animal and human
    studies, that supports possible immune-mediated mechanisms underlying the
    etiology of ASD.
    
    Copyright © 2014. Published by Elsevier Inc.
    
    PMID: 25218900  [PubMed - as supplied by publisher]
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  • 18) J Autism Dev Disord. 2014 Sep 14. [Epub ahead of print]

    Varieties of Misdiagnosis in ASD: An Illustrative Case Series.

    Van Schalkwyk GI(1), Peluso F, Qayyum Z, McPartland JC, Volkmar FR.
    
    Author information: 
    (1)Department of Psychiatry, Yale University, 9th Floor, 300 George St, New Haven,
    CT, 06511, USA, gerrit.vanschalkwyk@yale.edu.
    
    The relationship between autism spectrum disorders (ASD) and psychotic disorders 
    (PD) is a focus of continued interest. There are substantial conceptual and
    clinical difficulties associated with diagnosing comorbid PD in individuals who
    have ASD. In this case series, we report on five cases where adolescents with
    previously diagnosed ASD were also diagnosed as psychotic. In each case, we found
    that these patients' 'psychotic' symptoms could be better understood as a part of
    their underlying ASD diagnosis, with significant implications for treatment,
    prognosis, and access to services. This misdiagnosis likely represents a
    combination of adult psychiatrists being relatively inexperienced with this
    population, and the system of care requiring providers to apply diagnostic labels
    to justify inpatient hospitalization.
    
    PMID: 25218849  [PubMed - as supplied by publisher]
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  • 19) J Autism Dev Disord. 2014 Sep 14. [Epub ahead of print]

    Feasibility and Effectiveness of Very Early Intervention for Infants At-Risk for Autism Spectrum Disorder: A Systematic Review.

    Bradshaw J(1), Steiner AM, Gengoux G, Koegel LK.
    
    Author information: 
    (1)Counseling, Clinical, and School Psychology Department, Koegel Autism Center,
    Graduate School of Education, University of California, Santa Barbara, CA, USA,
    jbradshaw@education.ucsb.edu.
    
    Early detection methods for autism spectrum disorder (ASD) in infancy are rapidly
    advancing, yet the development of interventions for infants under two years with 
    or at-risk for ASD remains limited. In order to guide research and practice, this
    paper systematically reviewed studies investigating interventions for infants
    under 24 months with or at-risk for ASD. Nine studies were identified and
    evaluated for: (a) participants, (b) intervention approach (c) experimental
    design, and (d) outcomes. Studies that collected parent measures reported
    positive findings for parent acceptability, satisfaction, and improvement in
    parent implementation of treatment. Infant gains in social-communicative and
    developmental skills were observed following intervention in most of the reviewed
    studies, while comparisons with treatment-as-usual control groups elucidate the
    need for further research. These studies highlight the feasibility of very early 
    intervention and provide preliminary evidence that intervention for at-risk
    infants may be beneficial for infants and parents.
    
    PMID: 25218848  [PubMed - as supplied by publisher]
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  • 20) Nat Genet. 2014 Sep 14. doi: 10.1038/ng.3092. [Epub ahead of print]

    Refining analyses of copy number variation identifies specific genes associated with developmental delay.

    Coe BP(1), Witherspoon K(1), Rosenfeld JA(2), van Bon BW(3), Vulto-van Silfhout
    AT(4), Bosco P(5), Friend KL(6), Baker C(1), Buono S(5), Vissers LE(4),
    Schuurs-Hoeijmakers JH(4), Hoischen A(4), Pfundt R(4), Krumm N(1), Carvill GL(7),
    Li D(8), Amaral D(8), Brown N(9), Lockhart PJ(10), Scheffer IE(11), Alberti A(5),
    Shaw M(6), Pettinato R(5), Tervo R(12), de Leeuw N(4), Reijnders MR(4), Torchia
    BS(2), Peeters H(13), Thompson E(14), O'Roak BJ(15), Fichera M(16), Hehir-Kwa
    JY(4), Shendure J(1), Mefford HC(7), Haan E(14), Gécz J(17), de Vries BB(4),
    Romano C(5), Eichler EE(18).
    
    Author information: 
    (1)Department of Genome Sciences, University of Washington School of Medicine,
    Seattle, Washington, USA.
    (2)Signature Genomics Laboratories, LLC, PerkinElmer, Inc., Spokane, Washington,
    USA.
    (3)1] Department of Human Genetics, Radboud University Medical Center, Nijmegen, the
    Netherlands. [2] SA Pathology, North Adelaide, South Australia, Australia.
    (4)Department of Human Genetics, Radboud University Medical Center, Nijmegen, the
    Netherlands.
    (5)IRCCS (Istituto di Ricovero e Cura a Carattere Scientifico) Associazione Oasi
    Maria Santissima, Troina, Italy.
    (6)SA Pathology, North Adelaide, South Australia, Australia.
    (7)Department of Pediatrics, University of Washington, Seattle, Washington, USA.
    (8)Representing the Autism Phenome Project, MIND Institute, University of
    California, Davis, Sacramento, California, USA.
    (9)1] Department of Paediatrics, University of Melbourne, Royal Children's Hospital,
    Melbourne, Victoria, Australia. [2] Barwon Child Health Unit, Barwon Health,
    Geelong, Victoria, Australia.
    (10)1] Department of Paediatrics, University of Melbourne, Royal Children's Hospital,
    Melbourne, Victoria, Australia. [2] Murdoch Childrens Research Institute,
    University of Melbourne, Royal Children's Hospital, Melbourne, Victoria,
    Australia.
    (11)Florey Institute, University of Melbourne, Austin Health and Royal Children's
    Hospital, Melbourne, Victoria, Australia.
    (12)Division of Developmental and Behavioral Pediatrics, Mayo Clinic, Rochester,
    Minnesota, USA.
    (13)1] Center for Human Genetics, University Hospitals Leuven, KU Leuven, Leuven,
    Belgium. [2] Leuven Autism Research (LAuRes), Leuven, Belgium.
    (14)1] SA Pathology, North Adelaide, South Australia, Australia. [2] School of
    Paediatrics and Reproductive Health, University of Adelaide, Adelaide, South
    Australia, Australia.
    (15)1] Department of Genome Sciences, University of Washington School of Medicine,
    Seattle, Washington, USA. [2].
    (16)1] IRCCS (Istituto di Ricovero e Cura a Carattere Scientifico) Associazione Oasi 
    Maria Santissima, Troina, Italy. [2].
    (17)1] SA Pathology, North Adelaide, South Australia, Australia. [2] Robinson
    Institute, University of Adelaide, Adelaide, South Australia, Australia.
    (18)1] Department of Genome Sciences, University of Washington School of Medicine,
    Seattle, Washington, USA. [2] Howard Hughes Medical Institute, Seattle,
    Washington, USA.
    
    Copy number variants (CNVs) are associated with many neurocognitive disorders;
    however, these events are typically large, and the underlying causative genes are
    unclear. We created an expanded CNV morbidity map from 29,085 children with
    developmental delay in comparison to 19,584 healthy controls, identifying 70
    significant CNVs. We resequenced 26 candidate genes in 4,716 additional cases
    with developmental delay or autism and 2,193 controls. An integrated analysis of 
    CNV and single-nucleotide variant (SNV) data pinpointed 10 genes enriched for
    putative loss of function. Follow-up of a subset of affected individuals
    identified new clinical subtypes of pediatric disease and the genes responsible
    for disease-associated CNVs. These genetic changes include haploinsufficiency of 
    SETBP1 associated with intellectual disability and loss of expressive language
    and truncations of ZMYND11 in individuals with autism, aggression and complex
    neuropsychiatric features. This combined CNV and SNV approach facilitates the
    rapid discovery of new syndromes and genes involved in neuropsychiatric disease
    despite extensive genetic heterogeneity.
    
    PMID: 25217958  [PubMed - as supplied by publisher]
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