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Autistic Disorder: HELP
Articles from Minnesota
Based on 168 articles published since 2010
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These are the 168 published articles about Autistic Disorder that originated from Minnesota during 2010-2020.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7
1 Review The Role of Diagnostic Instruments in Dual and Differential Diagnosis in Autism Spectrum Disorder Across the Lifespan. 2020

Shulman, Cory / Rice, Catherine E / Morrier, Michael J / Esler, Amy. ·The Paul Baerwald School of Social Work and Social Welfare, The Hebrew University of Jerusalem, Mount Scopus, Jerusalem, 91905, Israel. Electronic address: cory.shulman@mail.huji.ac.il. · Emory Autism Center, 1551 Shoup Court, Department of Psychiatry & Behavioral Sciences, Emory University School of Medicine, Decatur, GA 30033, USA. · Division of Clinical Behavioral Neuroscience, Department of Pediatrics, University of Minnesota 2540 Riverside Ave S., RPB 550, Minneapolis, MN 55454, USA. ·Child Adolesc Psychiatr Clin N Am · Pubmed #32169263.

ABSTRACT: The heterogeneity inherent in autism spectrum disorder (ASD) makes the identification and diagnosis of ASD complex. We survey a large number of diagnostic tools, including screeners and tools designed for in-depth assessment. We also discuss the challenges presented by overlapping symptomatology between ASD and other disorders and the need to determine whether a diagnosis of ASD or another diagnosis best explains the individual's symptoms. We conclude with a call to action for the next steps necessary for meeting the diagnostic challenges presented here to improve the diagnostic process and to help understand each individual's particular ASD profile.

2 Review Diagnosis of Autism Spectrum Disorder Across the Lifespan. 2020

Shulman, Cory / Esler, Amy / Morrier, Michael J / Rice, Catherine E. ·The Paul Baerwald School of Social Work and Social Welfare, The Hebrew University of Jerusalem, Mount Scopus, Jerusalem, 91905, Israel. Electronic address: cory.shulman@mail.huji.ac.il. · Division of Clinical Behavioral Neuroscience, Department of Pediatrics, University of Minnesota 2540 Riverside Ave S., RPB 550, Minneapolis, MN 55454, USA. · Emory Autism Center, 1551 Shoup Court, Department of Psychiatry & Behavioral Sciences, Emory University School of Medicine, Decatur, GA 30033, USA. ·Child Adolesc Psychiatr Clin N Am · Pubmed #32169262.

ABSTRACT: Although autism spectrum disorder (ASD) is one of the most common neurodevelopmental disorders it is also one of the most heterogeneous conditions, making identification and diagnosis complex. The importance of a stable and consistent diagnosis cannot be overstated. An accurate diagnosis is the basis for understanding the individual and establishing an individualized treatment plan. We present those elements that should be included in any assessment for ASD and describe the ways in which ASD typically manifests itself at various developmental stages. The implications and challenges for assessment at different ages and levels of functioning are discussed.

3 Review Are school psychologists' special education eligibility decisions reliable and unbiased?: A multi-study experimental investigation. 2019

Sullivan, Amanda L / Sadeh, Shanna / Houri, Alaa K. ·Department of Educational Psychology, College of Education & Human Development, University of Minnesota, USA. Electronic address: asulliva@umn.edu. · Department of Educational Psychology, College of Education & Human Development, University of Minnesota, USA. ·J Sch Psychol · Pubmed #31837731.

ABSTRACT: Nearly 50 years of research show persistent racial disproportionality in the identification of special education disabilities, but the underlying mechanisms for these disparities remain largely unexplored. Because ambiguous regulations defining disabilities may allow subjectivity and unlawful differential treatment (i.e., racial bias or discrimination) in the special education eligibility process, an important target of study is disparate treatment of students by race in evaluations required to determine eligibility. School psychologists have long been recognized as highly influential in this process and in schools' resultant decisions. We used a 3 × 2 mixed factorial experimental design in three studies with simulated case report data to measure the influence of race and assessment data on school psychologists' perceptions of students' eligibility for special education in cases centering on emotional disturbance, intellectual disability, or autism, respectively. Participants included 302 practicing school psychologists in three states across the three experiments. There was little evidence of racial disparity, but participants tended to render decisions unsupported by, and even contrary to, evaluation data. Implications for research, practice, and professional development are discussed.

4 Review Microbiota transplant therapy and autism: lessons for the clinic. 2019

Adams, James B / Borody, Thomas J / Kang, Dae-Wook / Khoruts, Alexander / Krajmalnik-Brown, Rosa / Sadowsky, Michael J. ·School for Engineering of Matter, Transport, and Energy, Arizona State University, Tempe, Arizona, USA. · Centre for Digestive Diseases, Sydney, Australia. · Department of Civil & Environmental Engineering, The University of Toledo, Toledo, Ohio, USA. · Department of Medicine, Division of Gastroenterology; Center for Immunology, BioTechnology Institute, University of Minnesota, Minnepolis, Minnesota, USA. · Swette Center for Environmental Biotechnology, Arizona State University, Tempe, Arizona, USA. · BioTechnology Institute, and Departments of Soil, Water & Climate, and Plant& Microbial Biology, University of Minnesota, St. Paul, Minnesota, USA. ·Expert Rev Gastroenterol Hepatol · Pubmed #31665947.

ABSTRACT:

5 Review The co-occurrence of epilepsy and autism: A systematic review. 2019

Lukmanji, Sara / Manji, Sofiya A / Kadhim, Sandra / Sauro, Khara M / Wirrell, Elaine C / Kwon, Churl-Su / Jetté, Nathalie. ·Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Canada. · Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Canada; Department of Community Health Sciences, O'Brien Institute for Public Health, Cumming School of Medicine, University of Calgary, Calgary, Canada. · Child and Adolescent Neurology, Mayo Clinic, Rochester, MN, USA. · Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Population Health Science & Policy, Icahn School of Medicine at Mount Sinai, New York, NY, USA. · Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Population Health Science & Policy, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: nathalie.jette@mssm.edu. ·Epilepsy Behav · Pubmed #31398688.

ABSTRACT: OBJECTIVE: We aimed to review the literature to determine the incidence and prevalence of autism in epilepsy and epilepsy in autism, conditions that are often comorbid. METHODS: We adhered to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) standards, and the protocol was registered with PROSPERO. MEDLINE, Embase, PsycINFO, and the Cochrane Database of Systematic Reviews were searched from inception until July 4, 2016. Studies were included if they reported an incidence or prevalence of autism in epilepsy or epilepsy in autism. These estimates were described using mean, standard deviation, median, and interquartile range. RESULTS: Seventy-four studies reporting on 283,549 patients were included. The median overall period prevalence of epilepsy in people with autism was 12.1% while the median overall period prevalence of autism in people with epilepsy was 9.0% when including all population types. When excluding studies that investigated patients with syndromic epilepsy or developmental delay, the median overall period prevalence of epilepsy in people with autism was 11.2% while the median overall period prevalence of autism in people with epilepsy was 8.1%. We observed trends for sex as the prevalence of autism in epilepsy was higher in males while the prevalence of epilepsy in autism was higher in females. It is important to interpret these estimates with caution, as there was significant heterogeneity between studies. Meta-regression found no association between study quality and prevalence or incidence estimates (all p-values > 0.05). CONCLUSIONS: The period prevalence of epilepsy in people with autism, and vice versa, was consistently higher than previously reported estimates of the occurrence of these disorders in the general population. These findings highlight the importance of screening for autism in people who have epilepsy and epilepsy in people who have autism and may help shed light on shared pathogenesis between these conditions.

6 Review Therapeutic Applications of Noninvasive Neuromodulation in Children and Adolescents. 2018

Doruk Camsari, Deniz / Kirkovski, Melissa / Croarkin, Paul E. ·Department of Psychiatry and Psychology, Mayo Clinic, 200 First Street Southwest, Rochester, MN 55905, USA. · Deakin Child Study Centre, School of Psychology, Deakin University, Geelong, VIC 3220, Australia. · Department of Psychiatry and Psychology, Mayo Clinic, 200 First Street Southwest, Rochester, MN 55905, USA. Electronic address: croarkin.paul@mayo.edu. ·Psychiatr Clin North Am · Pubmed #30098658.

ABSTRACT: Recent advances and growing evidence supporting the safety and efficacy of noninvasive neuromodulatory techniques in adults have facilitated the study of neuromodulation applications in children and adolescents. Noninvasive brain stimulation methods such as transcranial direct current stimulation and transcranial magnetic stimulation have been considered in children with depression, autism spectrum disorder, attention-deficit hyperactivity disorder, and other neuropsychiatric disorders. However, current clinical applications of neuromodulation techniques in children and adolescents are nascent. There is a great need for developmentally informed, large, double-blinded, randomized, controlled clinical trials to demonstrate efficacy and safety of noninvasive brain stimulation in children and adolescents.

7 Review Toward a conceptual framework for early brain and behavior development in autism. 2017

Piven, J / Elison, J T / Zylka, M J. ·Carolina Institute for Developmental Disabilities, The University of North Carolina, Chapel Hill, NC, USA. · Department of Psychiatry, The University of North Carolina, Chapel Hill, NC, USA. · Institute of Child Development and Department of Pediatrics, University of Minnesota, Minneapolis, MN, USA. · Department of Cell Biology and Physiology, and UNC Neuroscience Center, The University of North Carolina, Chapel Hill, NC, USA. ·Mol Psychiatry · Pubmed #28937691.

ABSTRACT: Studies of infant siblings of older autistic probands, who are at elevated risk for autism, have demonstrated that the defining features of autism are not present in the first year of life but emerge late in the first and into the second year. A recent longitudinal neuroimaging study of high-risk siblings revealed a specific pattern of brain development in infants later diagnosed with autism, characterized by cortical surface area hyper-expansion in the first year followed by brain volume overgrowth in the second year that is associated with the emergence of autistic social deficits. Together with new observations from genetically defined autism risk alleles and rodent model, these findings suggest a conceptual framework for the early, post-natal development of autism. This framework postulates that an increase in the proliferation of neural progenitor cells and hyper-expansion of cortical surface area in the first year, occurring during a pre-symptomatic period characterized by disrupted sensorimotor and attentional experience, leads to altered experience-dependent neuronal development and decreased elimination of neuronal processes. This process is linked to brain volume overgrowth and disruption of the refinement of neural circuit connections and is associated with the emergence of autistic social deficits in the second year of life. A better understanding of the timing of developmental brain and behavior mechanisms in autism during infancy, a period which precedes the emergence of the defining features of this disorder, will likely have important implications for designing rational approaches to early intervention.

8 Review Pharmacogenomics of autism spectrum disorder. 2017

Brown, Jacob T / Eum, Seenae / Cook, Edwin H / Bishop, Jeffrey R. ·Department of Pharmacy Practice & Pharmaceutical Sciences, College of Pharmacy, University of Minnesota, Duluth, MN, USA. · Department of Experimental & Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, MN, USA. · Department of Psychiatry, College of Medicine, University of Illinois at Chicago, Chicago, IL, USA. · Department of Psychiatry, College of Medicine, University of Minnesota, Minneapolis, MN, USA. ·Pharmacogenomics · Pubmed #28244813.

ABSTRACT: Autism spectrum disorder (ASD) is characterized by persistent deficits in social communication and interactions as well as restricted, repetitive behaviors and interests. Pharmacologic interventions are often needed to manage irritability, aggressive behaviors and hyperactivity. Pharmacogenomic studies have investigated genetic associations with treatment response and side effects in an attempt to better understand drug mechanisms in hopes of optimizing the balance of symptom improvement versus side effects. The majority of pharmacogenomic studies to date have focused on antipsychotics, antidepressants and stimulants that are the most commonly utilized medication classes for ASD. This review is a comprehensive examination of the existing pharmacogenomic studies in ASD highlighting the current state of knowledge regarding genetic variation influencing pharmacokinetics and pharmacodynamics, and associated clinical outcomes.

9 Review Neuropathological Mechanisms of Seizures in Autism Spectrum Disorder. 2016

Frye, Richard E / Casanova, Manuel F / Fatemi, S Hossein / Folsom, Timothy D / Reutiman, Teri J / Brown, Gregory L / Edelson, Stephen M / Slattery, John C / Adams, James B. ·Autism Research Program, Arkansas Children's Research InstituteLittle Rock, AR, USA; Department of Pediatrics, University of Arkansas for Medical SciencesLittle Rock, AR, USA. · Department of Biomedical Sciences, University of South Carolina School of Medicine Greenville Greenville, SC, USA. · Department of Psychiatry, University of Minnesota Medical School Minneapolis, MN, USA. · Serenity Health Care Center Waukesha, WI, USA. · Autism Research Institute San Diego, CA, USA. · School for Engineering of Matter, Transport, and Energy, Arizona State University Tempe, AZ, USA. ·Front Neurosci · Pubmed #27242398.

ABSTRACT: This manuscript reviews biological abnormalities shared by autism spectrum disorder (ASD) and epilepsy. Two neuropathological findings are shared by ASD and epilepsy: abnormalities in minicolumn architecture and γ-aminobutyric acid (GABA) neurotransmission. The peripheral neuropil, which is the region that contains the inhibition circuits of the minicolumns, has been found to be decreased in the post-mortem ASD brain. ASD and epilepsy are associated with inhibitory GABA neurotransmission abnormalities including reduced GABAA and GABAB subunit expression. These abnormalities can elevate the excitation-to-inhibition balance, resulting in hyperexcitablity of the cortex and, in turn, increase the risk of seizures. Medical abnormalities associated with both epilepsy and ASD are discussed. These include specific genetic syndromes, specific metabolic disorders including disorders of energy metabolism and GABA and glutamate neurotransmission, mineral and vitamin deficiencies, heavy metal exposures and immune dysfunction. Many of these medical abnormalities can result in an elevation of the excitatory-to-inhibitory balance. Fragile X is linked to dysfunction of the mGluR5 receptor and Fragile X, Angelman and Rett syndromes are linked to a reduction in GABAA receptor expression. Defects in energy metabolism can reduce GABA interneuron function. Both pyridoxine dependent seizures and succinic semialdehyde dehydrogenase deficiency cause GABA deficiencies while urea cycle defects and phenylketonuria cause abnormalities in glutamate neurotransmission. Mineral deficiencies can cause glutamate and GABA neurotransmission abnormalities and heavy metals can cause mitochondrial dysfunction which disrupts GABA metabolism. Thus, both ASD and epilepsy are associated with similar abnormalities that may alter the excitatory-to-inhibitory balance of the cortex. These parallels may explain the high prevalence of epilepsy in ASD and the elevated prevalence of ASD features in individuals with epilepsy.

10 Review Understanding autism and other neurodevelopmental disorders through experimental translational neurobehavioral models. 2016

Homberg, Judith R / Kyzar, Evan J / Nguyen, Michael / Norton, William H / Pittman, Julian / Poudel, Manoj K / Gaikwad, Siddharth / Nakamura, Shun / Koshiba, Mamiko / Yamanouchi, Hideo / Scattoni, Maria Luisa / Ullman, Jeremy F P / Diamond, David M / Kaluyeva, Aleksandra A / Parker, Matthew O / Klimenko, Victor M / Apryatin, Sergey A / Brown, Richard E / Song, Cai / Gainetdinov, Raul R / Gottesman, Irving I / Kalueff, Allan V. ·Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition, and Behaviour, Radboud University Medical Centre, Nijmegen, Netherlands. · Department of Psychiatry, College of Medicine, University of Illinois at Chicago, Chicago, IL, USA; The International Stress and Behavior Society (ISBS) and ZENEREI Research Center, Slidell, LA, USA. · The International Stress and Behavior Society (ISBS) and ZENEREI Research Center, Slidell, LA, USA; New York University School of Medicine, NY, NY, USA. · Department of Biology, University of Leicester, Leicester, UK. · Department of Biological and Environmental Sciences, Troy University, Troy, AL, USA. · The International Stress and Behavior Society (ISBS) and ZENEREI Research Center, Slidell, LA, USA. · Tokyo University of Agriculture and Technology, Tokyo, Japan. · Departments of Pediatrics and Biochemistry, Saitama Medical University, Saitama, Japan. · Department of Cell Biology and Neurosciences, Istituto Superiore di Sanita, Rome, Italy. · Centre for Advanced Imaging, University of Queensland, Brisbane, Queensland, Australia. · Department of Psychology, University of South Florida, Tampa, FL, USA; J.A. Haley Veterans Hospital, Research and Development Service, Tampa, FL, USA. · School of Health Sciences and Social Work, University of Portsmouth, Portsmouth, UK. · Pavlov Physiology Department, Institute of Experimental Medicine IEM RAS, St. Petersburg, Russia. · Research Institute of Nutrition RAS, Moscow, Russia. · Department of Psychology and Neuroscience, Dalhousie University, Halifax, Nova Scotia, Canada. · Department of Psychology and Neuroscience, Dalhousie University, Halifax, Nova Scotia, Canada; Research Institute of Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang, Guangdong, China; Graduate Neuroscience Institute, China Medical University Hospital, Taichung, Taiwan. · Institute of Translational Biomedicine, St. Petersburg State University, St. Petersburg, Russia; Skolkovo Institute of Science and Technology, Skolkovo, Moscow Region, Russia. · Department of Psychology, University of Minnesota, Minneapolis, MN, USA. · Research Institute of Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang, Guangdong, China; Institute of Translational Biomedicine, St. Petersburg State University, St. Petersburg, Russia; Institutes of Chemical Technology and Natural Sciences, Ural Federal University, Ekaterinburg, Russia. Electronic address: avkalueff@gmail.com. ·Neurosci Biobehav Rev · Pubmed #27048961.

ABSTRACT: Neurodevelopmental disorders (NDDs) are highly prevalent and severely debilitating brain illnesses caused by aberrant brain growth and development. Resulting in cognitive, social, motor, language and affective disabilities, common NDDs include autism spectrum disorder (ASD), intellectual disability, communication/speech disorders, motor/tic disorders and attention deficit hyperactivity disorder. Affecting neurogenesis, glia/neuronal proliferation and migration, synapse formation and myelination, aberrant neural development occurs over a substantial period of time. Genetic, epigenetic, and environmental factors play a key role in NDD pathogenesis. Animal models are an indispensable tool to study NDDs. Paralleling clinical findings, we comprehensively evaluate various preclinical tests and models which target key (social, cognitive, motor) neurobehavioral domains of ASD and other common NDDs. Covering both traditional (rodent) and alternative NDD models, we outline the emerging areas of research and emphasize how preclinical models play a key role in gaining translational and mechanistic insights into NDDs and their therapy.

11 Review Autism Spectrum Disorders and Drug Addiction: Common Pathways, Common Molecules, Distinct Disorders? 2016

Rothwell, Patrick E. ·Department of Neuroscience, University of Minnesota Minneapolis, MN, USA. ·Front Neurosci · Pubmed #26903789.

ABSTRACT: Autism spectrum disorders (ASDs) and drug addiction do not share substantial comorbidity or obvious similarities in etiology or symptomatology. It is thus surprising that a number of recent studies implicate overlapping neural circuits and molecular signaling pathways in both disorders. The purpose of this review is to highlight this emerging intersection and consider implications for understanding the pathophysiology of these seemingly distinct disorders. One area of overlap involves neural circuits and neuromodulatory systems in the striatum and basal ganglia, which play an established role in addiction and reward but are increasingly implicated in clinical and preclinical studies of ASDs. A second area of overlap relates to molecules like Fragile X mental retardation protein (FMRP) and methyl CpG-binding protein-2 (MECP2), which are best known for their contribution to the pathogenesis of syndromic ASDs, but have recently been shown to regulate behavioral and neurobiological responses to addictive drug exposure. These shared pathways and molecules point to common dimensions of behavioral dysfunction, including the repetition of behavioral patterns and aberrant reward processing. The synthesis of knowledge gained through parallel investigations of ASDs and addiction may inspire the design of new therapeutic interventions to correct common elements of striatal dysfunction.

12 Review GABA receptor subunit distribution and FMRP-mGluR5 signaling abnormalities in the cerebellum of subjects with schizophrenia, mood disorders, and autism. 2015

Fatemi, S Hossein / Folsom, Timothy D. ·Department of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St SE, MMC 392, Minneapolis, MN 55455, USA; Department of Neuroscience, University of Minnesota Medical School, 321 Church St. SE, Minneapolis, MN 55455, USA. Electronic address: fatem002@umn.edu. · Department of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St SE, MMC 392, Minneapolis, MN 55455, USA. Electronic address: folso013@umn.edu. ·Schizophr Res · Pubmed #25432637.

ABSTRACT: Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the brain. GABAergic receptor abnormalities have been documented in several major psychiatric disorders including schizophrenia, mood disorders, and autism. Abnormal expression of mRNA and protein for multiple GABA receptors has also been observed in multiple brain regions leading to alterations in the balance between excitatory/inhibitory signaling in the brain with potential profound consequences for normal cognition and maintenance of mood and perception. Altered expression of GABAA receptor subunits has been documented in fragile X mental retardation 1 (FMR1) knockout mice, suggesting that loss of its protein product, fragile X mental retardation protein (FMRP), impacts GABAA subunit expression. Recent postmortem studies from our laboratory have shown reduced expression of FMRP in the brains of subjects with schizophrenia, bipolar disorder, major depression, and autism. FMRP acts as a translational repressor and, under normal conditions, inhibits metabotropic glutamate receptor 5 (mGluR5)-mediated signaling. In fragile X syndrome (FXS), the absence of FMRP is hypothesized to lead to unregulated mGluR5 signaling, ultimately resulting in the behavioral and intellectual impairments associated with this disorder. Our laboratory has identified changes in mGluR5 expression in autism, schizophrenia, and mood disorders. In the current review article, we discuss our postmortem data on GABA receptors, FMRP, and mGluR5 levels and compare our results with other laboratories. Finally, we discuss the interactions between these molecules and the potential for new therapeutic interventions that target these interconnected signaling systems.

13 Review Learning how to be a student: an overview of instructional practices targeting school readiness skills for preschoolers with autism spectrum disorder. 2015

Fleury, Veronica P / Thompson, Julie L / Wong, Connie. ·University of Minnesota, Minneapolis, USA vpfleury@umn.edu. · University of North Carolina at Charlotte, USA. · University of North Carolina at Chapel Hill, USA. ·Behav Modif · Pubmed #25261082.

ABSTRACT: Due to difficulties associated with autism spectrum disorder (ASD), many children with ASD will require additional support to actively participate in classroom activities. Therefore, it is important that professionals who work with young children with ASD know what skills to teach and how to teach them. Using the recent evidence-based practice review conducted by the National Professional Development Center on ASD, we have identified studies that targeted school readiness behaviors which can have implications for academic skill development. In this article, we evaluate (a) the types of skills that have been taught to preschool children with ASD, (b) the strategies used to teach specific skills, and (c) other descriptive information, such as who delivered the intervention and the setting in which the intervention took place. We conclude by offering suggestions for future research and considerations for professional development.

14 Review Intranasal oxytocin in the treatment of autism spectrum disorders: a review of literature and early safety and efficacy data in youth. 2014

Anagnostou, Evdokia / Soorya, Latha / Brian, Jessica / Dupuis, Annie / Mankad, Deepali / Smile, Sharon / Jacob, Suma. ·Bloorview Research Institute, University of Toronto, 150 Kilgour Road, Toronto, ON, Canada M4G 1R8. Electronic address: eanagnostou@hollandbloorview.ca. · Rush University Medical Center, Department of Psychiatry, 2150 West Harrison Street, Chicago, IL 606103, USA. · Bloorview Research Institute, University of Toronto, 150 Kilgour Road, Toronto, ON, Canada M4G 1R8. · The Hospital for Sick Children, Dalla Lana School of Public Health, University of Toronto, 555 University Avenue, Toronto, Canada M5G 1X8. · University of Minnesota, Department of Psychiatry & Pediatrics, 2101 6th Street SE, Minneapolis, MN 55455, USA. ·Brain Res · Pubmed #24508578.

ABSTRACT: BACKGROUND: There is a paucity of treatments targeting core symptom domains in Autism Spectrum Disorder (ASD). Several animal models and research in typically developing volunteers suggests that manipulation of the oxytocin system may have therapeutic potential for the treatment of social deficits. We review the literature for oxytocin and ASD and report on early dosing, safety and efficacy data of multi-dose oxytocin on aspects of social cognition/function, as well as repetitive behaviors and co-occurring anxiety within ASD. METHODS: Fifteen children and adolescents with verbal IQs≥70 were diagnosed with ASD using the ADOS and the ADI-R. They participated in a modified maximum tolerated dose study of intranasal oxytocin (Syntocinon). Data were modeled using repeated measures regression analysis controlling for week, dose, age, and sex. RESULTS: Among 4 doses tested, the highest dose evaluated, 0.4 IU/kg/dose, was found to be well tolerated. No serious or severe adverse events were reported and adverse events reported/observed were mild to moderate. Over 12 weeks of treatment, several measures of social cognition/function, repetitive behaviors and anxiety showed sensitivity to change with some measures suggesting maintenance of effect 3 months past discontinuation of intranasal oxytocin. CONCLUSIONS: This pilot study suggests that daily administration of intranasal oxytocin at 0.4 IU/kg/dose in children and adolescents with ASD is safe and has therapeutic potential. Larger studies are warranted. This article is part of a Special Issue entitled Oxytocin and Social Behav.

15 Review Oxytocin and vasopressin systems in genetic syndromes and neurodevelopmental disorders. 2014

Francis, S M / Sagar, A / Levin-Decanini, T / Liu, W / Carter, C S / Jacob, S. ·University of Minnesota, Department of Psychiatry, Minneapolis, MN, USA. · University of California at Irvine, Department of Psychiatry and Human Behavior, USA. · Northwestern University, Feinberg School of Medicine, Chicago, IL, USA. · University of North Carolina, Department of Psychiatry, Chapel Hill, NC, USA. · University of Minnesota, Department of Psychiatry, Minneapolis, MN, USA. Electronic address: sjacob@umn.edu. ·Brain Res · Pubmed #24462936.

ABSTRACT: Oxytocin (OT) and arginine vasopressin (AVP) are two small, related neuropeptide hormones found in many mammalian species, including humans. Dysregulation of these neuropeptides have been associated with changes in behavior, especially social interactions. We review how the OT and AVP systems have been investigated in Autism Spectrum Disorder (ASD), Prader-Willi Syndrome (PWS), Williams Syndrome (WS) and Fragile X syndrome (FXS). All of these neurodevelopmental disorders (NDD) are marked by social deficits. While PWS, WS and FXS have identified genetic mutations, ASD stems from multiple genes with complex interactions. Animal models of NDD are invaluable for studying the role and relatedness of OT and AVP in the developing brain. We present data from a FXS mouse model affecting the fragile X mental retardation 1 (Fmr1) gene, resulting in decreased OT and AVP staining cells in some brain regions. Reviewing the research about OT and AVP in these NDD suggests that altered OT pathways may be downstream from different etiological factors and perturbations in development. This has implications for ongoing studies of the therapeutic application of OT in NDD. This article is part of a Special Issue entitled Oxytocin and Social Behav.

16 Review A review of traditional and novel treatments for seizures in autism spectrum disorder: findings from a systematic review and expert panel. 2013

Frye, Richard E / Rossignol, Daniel / Casanova, Manuel F / Brown, Gregory L / Martin, Victoria / Edelson, Stephen / Coben, Robert / Lewine, Jeffrey / Slattery, John C / Lau, Chrystal / Hardy, Paul / Fatemi, S Hossein / Folsom, Timothy D / Macfabe, Derrick / Adams, James B. ·Arkansas Children's Hospital Research Institute , Little Rock, AR , USA. · Rossignol Medical Center , Irvine, CA , USA. · University of Louisville , Louisville, KY , USA. · Autism Recovery and Comprehensive Health Medical Center , Franklin, WI , USA. · Autism Research Institute , San Diego, CA , USA. · New York University Brain Research Laboratory , New York, NY , USA. · MIND Research Network, University of New Mexico , Albuquerque, NM , USA. · Hardy Healthcare Associates , Hingham, MA , USA. · University of Minnesota Medical School , Minneapolis, MN , USA. · University of Western Ontario , London, ON , Canada. · Arizona State University , Tempe, AZ , USA. ·Front Public Health · Pubmed #24350200.

ABSTRACT: Despite the fact that seizures are commonly associated with autism spectrum disorder (ASD), the effectiveness of treatments for seizures has not been well studied in individuals with ASD. This manuscript reviews both traditional and novel treatments for seizures associated with ASD. Studies were selected by systematically searching major electronic databases and by a panel of experts that treat ASD individuals. Only a few anti-epileptic drugs (AEDs) have undergone carefully controlled trials in ASD, but these trials examined outcomes other than seizures. Several lines of evidence point to valproate, lamotrigine, and levetiracetam as the most effective and tolerable AEDs for individuals with ASD. Limited evidence supports the use of traditional non-AED treatments, such as the ketogenic and modified Atkins diet, multiple subpial transections, immunomodulation, and neurofeedback treatments. Although specific treatments may be more appropriate for specific genetic and metabolic syndromes associated with ASD and seizures, there are few studies which have documented the effectiveness of treatments for seizures for specific syndromes. Limited evidence supports l-carnitine, multivitamins, and N-acetyl-l-cysteine in mitochondrial disease and dysfunction, folinic acid in cerebral folate abnormalities and early treatment with vigabatrin in tuberous sclerosis complex. Finally, there is limited evidence for a number of novel treatments, particularly magnesium with pyridoxine, omega-3 fatty acids, the gluten-free casein-free diet, and low-frequency repetitive transcranial magnetic simulation. Zinc and l-carnosine are potential novel treatments supported by basic research but not clinical studies. This review demonstrates the wide variety of treatments used to treat seizures in individuals with ASD as well as the striking lack of clinical trials performed to support the use of these treatments. Additional studies concerning these treatments for controlling seizures in individuals with ASD are warranted.

17 Review Story and science: how providers and parents can utilize storytelling to combat anti-vaccine misinformation. 2013

Shelby, Ashley / Ernst, Karen. ·Moms Who Vax; Twin Cities, MN USA. ·Hum Vaccin Immunother · Pubmed #23811786.

ABSTRACT: With little or no evidence-based information to back up claims of vaccine danger, anti-vaccine activists have relied on the power of storytelling to infect an entire generation of parents with fear of and doubt about vaccines. These parent accounts of perceived vaccine injury, coupled with Andrew Wakefield's fraudulent research study linking the MMR vaccine to autism, created a substantial amount of vaccine hesitancy in new parents, which manifests in both vaccine refusal and the adoption of delayed vaccine schedules. The tools used by the medical and public health communities to counteract the anti-vaccine movement include statistics, research, and other evidence-based information, often delivered verbally or in the form of the CDC's Vaccine Information Statements. This approach may not be effective enough on its own to convince vaccine-hesitant parents that vaccines are safe, effective, and crucial to their children's health. Utilizing some of the storytelling strategies used by the anti-vaccine movement, in addition to evidence-based vaccine information, could potentially offer providers, public health officials, and pro-vaccine parents an opportunity to mount a much stronger defense against anti-vaccine messaging.

18 Review Proton magnetic resonance spectroscopy as a probe into the pathophysiology of autism spectrum disorders (ASD): a review. 2013

Baruth, Joshua M / Wall, Christopher A / Patterson, Marc C / Port, John D. ·Department of Psychiatry and Psychology, Mayo Clinic, Rochester, Minnesota 55905, USA. jmbaru01@louisville.edu ·Autism Res · Pubmed #23436782.

ABSTRACT: Proton magnetic resonance spectroscopy ((1) H-MRS) is a safe, noninvasive way of quantifying in vivo biochemical and metabolite concentration levels in individuals with Autism Spectrum Disorders (ASD). Findings to date suggest ASD is associated with widespread reduction in N-acetylaspartate (NAA), creatine plus phosphocreatine (Cr), choline-containing compounds (Cho), myo-inositol (mI), and glutamate plus glutamine plus gamma-Aminobutyric Acid (Glx); however, variable findings, and even substantial increases, are not uncommon depending on the study and/or region-of-interest. Widespread reduction of NAA, Cr, Cho, mI, and Glx in ASD likely reflects impaired neuronal function and/or metabolism related to abnormal neurodevelopmental processes. Future studies should attempt to relate (1) H-MRS findings to histological findings and control for variability in subject age and functioning level; this would assist in evaluating the relationship between (1) H-MRS metabolic levels and neuronal and glial cell densities, as well as neurodevelopmental process associated with ASD. Furthermore, more longitudinal (1) H-MRS studies are needed in both control and ASD subjects to attempt to standardize metabolite levels across different developmental periods in well-defined endophenotypes. This will provide for a standard rubric for which metabolic aberrations (as well as treatment responses) can be measured. With higher magnetic field strengths and spectral-editing techniques capable of quantifying less-concentrated metabolites, (1) H-MRS will continue to be an important tool in ASD research.

19 Review Autism research and services for young children: history, progress and challenges. 2013

Thompson, Travis. ·Special Education Program, Department of Educational Psychology, University of Minnesota, Minneapolis, MN, USA. thomp199@umn.edu ·J Appl Res Intellect Disabil · Pubmed #23404617.

ABSTRACT: For three decades after Leo Kanner's first clinical description, research progress in understanding and treating autism was minimal but since the late 1960s the growth of autism discoveries has been exponential, with a remarkable number of new findings published over the past two decades, in particular. These advances were made possible first by the discovery and dissemination of early intensive behavioural intervention (EIBI) for young children with autism that created the impetus for earlier accurate diagnosis. Other factors influencing the rapid growth in autism research were the first accepted diagnostic test for autism, the Autism Diagnostic Interview and Observation Schedule (ADI and ADOS). Developments in brain imaging and genetic technology combined to create a fuller understanding of the heterogeneity of autism, its multiple aetiologies, very early onset and course, and strategies for treatment. For a significant proportion of children with autism, it appears EIBI may be capable of promoting brain connectivity in specific cerebral areas, which is one of autism's underlying challenges. Disagreements about the most appropriate early intervention approach between developmental and behavioural psychologists have been unproductive and not contributed to advancing the field. Naturalistic behavioural and structured discrete trial methods are being integrated with developmental strategies with promising outcomes. Over these past 30 years, young people with autism have gone from receiving essentially no proactive treatment, resulting in lives languishing in institutions, to today, when half of children receiving EIBI treatment subsequently participate in regular classrooms alongside their peers. The future has entirely changed for young people with autism. Autism has become an eminently treatable condition. The time is overdue to set aside philosophical quarrels regarding theories of child development and apply what we know for the benefit of children with autism and their families.

20 Review The involvement of Reelin in neurodevelopmental disorders. 2013

Folsom, Timothy D / Fatemi, S Hossein. ·Department of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St. SE, MMC 392, Minneapolis, MN 55455, USA. folso013@umn.edu ·Neuropharmacology · Pubmed #22981949.

ABSTRACT: Reelin is a glycoprotein that serves important roles both during development (regulation of neuronal migration and brain lamination) and in adulthood (maintenance of synaptic function). A number of neuropsychiatric disorders including autism, schizophrenia, bipolar disorder, major depression, Alzheimer's disease and lissencephaly share a common feature of abnormal Reelin expression in the brain. Altered Reelin expression has been hypothesized to impair neuronal connectivity and synaptic plasticity, leading ultimately to the cognitive deficits present in these disorders. The mechanisms for abnormal Reelin expression in some of these disorders are currently unknown although possible explanations include early developmental insults, mutations, hypermethylation of the promoter for the Reelin gene (RELN), miRNA silencing of Reelin mRNA, FMRP underexpression and Reelin processing abnormalities. Increasing Reelin expression through pharmacological therapies may help ameliorate symptoms resulting from Reelin deficits. This article is part of the Special Issue entitled 'Neurodevelopmental Disorders'.

21 Review Consensus paper: pathological role of the cerebellum in autism. 2012

Fatemi, S Hossein / Aldinger, Kimberly A / Ashwood, Paul / Bauman, Margaret L / Blaha, Charles D / Blatt, Gene J / Chauhan, Abha / Chauhan, Ved / Dager, Stephen R / Dickson, Price E / Estes, Annette M / Goldowitz, Dan / Heck, Detlef H / Kemper, Thomas L / King, Bryan H / Martin, Loren A / Millen, Kathleen J / Mittleman, Guy / Mosconi, Matthew W / Persico, Antonio M / Sweeney, John A / Webb, Sara J / Welsh, John P. ·University of Minnesota Medical School, 420 Delaware St. SE, Minneapolis, MN 55455, USA. fatem002@umn.edu ·Cerebellum · Pubmed #22370873.

ABSTRACT: There has been significant advancement in various aspects of scientific knowledge concerning the role of cerebellum in the etiopathogenesis of autism. In the current consensus paper, we will observe the diversity of opinions regarding the involvement of this important site in the pathology of autism. Recent emergent findings in literature related to cerebellar involvement in autism are discussed, including: cerebellar pathology, cerebellar imaging and symptom expression in autism, cerebellar genetics, cerebellar immune function, oxidative stress and mitochondrial dysfunction, GABAergic and glutamatergic systems, cholinergic, dopaminergic, serotonergic, and oxytocin-related changes in autism, motor control and cognitive deficits, cerebellar coordination of movements and cognition, gene-environment interactions, therapeutics in autism, and relevant animal models of autism. Points of consensus include presence of abnormal cerebellar anatomy, abnormal neurotransmitter systems, oxidative stress, cerebellar motor and cognitive deficits, and neuroinflammation in subjects with autism. Undefined areas or areas requiring further investigation include lack of treatment options for core symptoms of autism, vermal hypoplasia, and other vermal abnormalities as a consistent feature of autism, mechanisms underlying cerebellar contributions to cognition, and unknown mechanisms underlying neuroinflammation.

22 Review Applications of transcranial magnetic stimulation (TMS) in child and adolescent psychiatry. 2011

Croarkin, Paul E / Wall, Christopher A / Lee, Jon. ·Mayo Clinic, Rochester, Minnesota, USA. Croarkin.paul@mayo.edu ·Int Rev Psychiatry · Pubmed #22200134.

ABSTRACT: Transcranial magnetic stimulation (TMS) is emerging as a new treatment and neurophysiological research tool for psychiatric disorders. Recent publications suggest that this modality will also serve as a treatment and research tool in child and adolescent psychiatry. Current reports on therapeutic trials of repetitive transcranial magnetic stimulation (rTMS) in adolescents have primarily focused on depression. However, other pilot work involves the treatment of attention-deficit/hyperactivity disorder (ADHD), autism and schizophrenia. Neurophysiological studies typically utilize single and paired-pulse TMS paradigms which index cortical excitability and inhibition. Initial studies have focused on ADHD, autism, and depression. General knowledge regarding TMS among child and adolescent psychiatrists is lacking. The aim of this review is to provide an overview of TMS in the context of child and adolescent psychiatry, discuss recent therapeutic and neurophysiological studies, and examine relevant ethical considerations.

23 Review The role of fragile X mental retardation protein in major mental disorders. 2011

Fatemi, S Hossein / Folsom, Timothy D. ·Department of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St SE, MMC 392, Minneapolis, MN 55455, USA. fatem002@umn.edu ·Neuropharmacology · Pubmed #21108954.

ABSTRACT: Fragile X mental retardation protein (FMRP) is highly enriched in neurons and binds to approximately 4% of mRNAs in mammalian brain. Its loss is a hallmark of fragile X syndrome (FXS), the most common form of mental retardation. In this review we discuss the mutation in the fragile X mental retardation-1 gene (FMR1), that leads to FXS, the role FMRP plays in neuronal cells, experiments from our own laboratory that demonstrate reductions of FMRP in additional psychiatric disorders (autism, schizophrenia, bipolar disorder, and major depressive disorder), and potential therapies to ameliorate the loss of FMRP. This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'.

24 Clinical Trial Microbiota Transfer Therapy alters gut ecosystem and improves gastrointestinal and autism symptoms: an open-label study. 2017

Kang, Dae-Wook / Adams, James B / Gregory, Ann C / Borody, Thomas / Chittick, Lauren / Fasano, Alessio / Khoruts, Alexander / Geis, Elizabeth / Maldonado, Juan / McDonough-Means, Sharon / Pollard, Elena L / Roux, Simon / Sadowsky, Michael J / Lipson, Karen Schwarzberg / Sullivan, Matthew B / Caporaso, J Gregory / Krajmalnik-Brown, Rosa. ·Biodesign Swette Center for Environmental Biotechnology, Arizona State University, Tempe, AZ, 85287, USA. · School for Engineering of Matter, Transport and Energy, Arizona State University, Tempe, AZ, 85287, USA. · Soil, Water and Environmental Sciences, University of Arizona, Tucson, AZ, 85721, USA. · Department of Microbiology, Ohio State University, Columbus, OH, 43210, USA. · Centre for Digestive Diseases, Five Dock, NSW, 2046, Australia. · Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ, 85287, USA. · Mucosal Immunology and Biology Research Center, Massachusetts General Hospital for Children, Boston, MA, 02114, USA. · Division of Gastroenterology, Department of Medicine, University of Minnesota, Minneapolis, MN, 55455, USA. · BioTechnology Institute, University of Minnesota, St. Paul, MN, 55108, USA. · Center for Immunology, University of Minnesota, Minneapolis, MN, 55414, USA. · Integrative Developmental Pediatrics, Tucson, AZ, 85701, USA. · Department of Soil, Water and Climate, University of Minnesota, St. Paul, MN, 55108, USA. · Pathogen and Microbiome Institute, Northern Arizona University, Flagstaff, AZ, 86011, USA. · Soil, Water and Environmental Sciences, University of Arizona, Tucson, AZ, 85721, USA. mbsulli@gmail.com. · Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ, 85287, USA. mbsulli@gmail.com. · Department of Microbiology, Ohio State University, Columbus, OH, 43210, USA. mbsulli@gmail.com. · Department of Civil, Environmental and Geodetic Engineering, Ohio State University, Columbus, OH, 43120, USA. mbsulli@gmail.com. · Pathogen and Microbiome Institute, Northern Arizona University, Flagstaff, AZ, 86011, USA. gregcaporaso@gmail.com. · Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ, 86011, USA. gregcaporaso@gmail.com. · Biodesign Swette Center for Environmental Biotechnology, Arizona State University, Tempe, AZ, 85287, USA. Dr.Rosy@asu.edu. · School of Sustainable Engineering and the Built Environment, Arizona State University, Tempe, AZ, 85287, USA. Dr.Rosy@asu.edu. ·Microbiome · Pubmed #28122648.

ABSTRACT: BACKGROUND: Autism spectrum disorders (ASD) are complex neurobiological disorders that impair social interactions and communication and lead to restricted, repetitive, and stereotyped patterns of behavior, interests, and activities. The causes of these disorders remain poorly understood, but gut microbiota, the 10 RESULTS: MTT involved a 2-week antibiotic treatment, a bowel cleanse, and then an extended fecal microbiota transplant (FMT) using a high initial dose followed by daily and lower maintenance doses for 7-8 weeks. The Gastrointestinal Symptom Rating Scale revealed an approximately 80% reduction of GI symptoms at the end of treatment, including significant improvements in symptoms of constipation, diarrhea, indigestion, and abdominal pain. Improvements persisted 8 weeks after treatment. Similarly, clinical assessments showed that behavioral ASD symptoms improved significantly and remained improved 8 weeks after treatment ended. Bacterial and phagedeep sequencing analyses revealed successful partial engraftment of donor microbiota and beneficial changes in the gut environment. Specifically, overall bacterial diversity and the abundance of Bifidobacterium, Prevotella, and Desulfovibrio among other taxa increased following MTT, and these changes persisted after treatment stopped (followed for 8 weeks). CONCLUSIONS: This exploratory, extended-duration treatment protocol thus appears to be a promising approach to alter the gut microbiome and virome and improve GI and behavioral symptoms of ASD. Improvements in GI symptoms, ASD symptoms, and the microbiome all persisted for at least 8 weeks after treatment ended, suggesting a long-term impact. TRIAL REGISTRATION: This trial was registered on the ClinicalTrials.gov, with the registration number  NCT02504554.

25 Article Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS) initially diagnosed as ALG6-CDG: Functional evidence for benignity of the ALG6 c.391T>C (p.Tyr131His) variant and further expanding the BBSOAS phenotype. 2020

Starosta, Rodrigo Tzovenos / Tarnowski, Jessica / Pinto E Vairo, Filippo / Raymond, Kimiyo / Preston, Graeme / Morava, Eva. ·Graduate Program in Genetics and Molecular Biology, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil; Department of Clinical Genomics, Mayo Clinic, Rochester, MN, USA. Electronic address: rodrigo.starosta@ufrgs.br. · Department of Clinical Genomics, Mayo Clinic, Rochester, MN, USA; Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA. · Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA. · Department of Clinical Genomics, Mayo Clinic, Rochester, MN, USA. ·Eur J Med Genet · Pubmed #32407885.

ABSTRACT: Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS) is a recently described autosomal dominant syndrome of developmental delay, cortical vision loss with optic nerve atrophy, epilepsy, and autism spectrum disorder. Due to its many overlapping features with congenital disorders of glycosylation (CDG), the differential diagnosis between these disorders may be difficult and relies on molecular genetic testing. We report on a 31-year-old female initially diagnosed with ALG6-CDG based on glycosylation abnormalities on transferrin isoelectrofocusing and mass spectrometry, and targeted genetic testing, and later diagnosed with BBSOAS by whole-exome sequencing (WES). Functional studies on cultured fibroblasts including Western blotting and RT-qPCR, as well as mass spectrometry of glycosylated transferrin and MALDI-TOF glycan analysis in serum, demonstrated normal glycosylation in this patient. In this report, we extend the phenotype of BBSOAS with ataxia and protein-losing enteropathy. This case is illustrative of the utility of whole exome sequencing in the diagnostic odyssey, and the potential pitfalls of relying on focused genetic testing results for diagnosis of conditions with complex overlapping phenotypes.

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