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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EAdvances in sequencing the entire human genome and large-scale genetic analyses have led to dramatically increased insights into neurodevelopmental disorders, including autism spectrum disorder (ASD) and intellectual disability (ID). Efforts are underway to use these insights to characterize the underlying molecular processes and functional pathways, with the goal of developing mechanism-based therapies for these disorders. This article provides an update on current approaches for the clinical and molecular genetic evaluation of individuals with ASD and ID, as well as discusses emerging treatments for neurodevelopmental disorders.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EPrevention \u0026amp; Screening\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ENeurodevelopmental Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EPrevention \u0026amp; Screening\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ENeurology\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ENeurodevelopmental Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EAdvances in sequencing the entire human genome and large-scale genetic analyses have led to dramatically increased insights into neurodevelopmental disorders, including autism spectrum disorder (ASD) and intellectual disability (ID). Efforts are underway to use these insights to characterize the underlying molecular processes and functional pathways, with the goal of developing mechanism-based therapies for these disorders.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EIn this session, Anna Szekely, MD, Yale University School of Medicine, New Haven, Connecticut, USA, provided an update on current approaches for the clinical and molecular genetic evaluation of individuals with ASD and ID. Francois V. Bolduc, MD, PhD, FRCPC, University of Alberta, Edmonton, Alberta, Canada, focused on emerging treatments for neurodevelopmental disorders that have been made possible by extensive characterization of the involved biological pathways.\u003C\/p\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EADVANCES IN GENOMIC TESTING ENHANCE UNDERSTANDING OF ASD\u003C\/h2\u003E\n         \u003Cp id=\u0022p-4\u0022\u003EASD represents a wide range of complex neurodevelopmental disorders resulting from multiple etiological factors. Dr. Szekely presented the new \u003Cem\u003EDiagnostic and Statistical Manual of Mental Disorders (DSM-5)\u003C\/em\u003E definition, which emphasizes that ASD is primarily characterized by deficits in social communication and interaction and restricted, repetitive patterns of behaviors, interests, or activities beginning in the early developmental period [American Psychiatric Association. ASD \u003Cem\u003EDSM-5.\u003C\/em\u003E 2013]. ID is common among children with ASD, with severe ID in about 50%, mild to moderate ID in 35%, and normal intellectual ability in 25% of affected children [Fombonne E. \u003Cem\u003EJ Clin Psychiatry\u003C\/em\u003E 2005].\u003C\/p\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EThe increasing incidence of ASD has spurred research on the wide phenotypic variability and highly heterogeneous genetics of these disorders. ASD is highly heritable, as shown in classical twin studies demonstrating 70% to 90% concordance in monozygotic twins [Bailey A et al. \u003Cem\u003EPsychol Med\u003C\/em\u003E 1995]. Other risk factors include male gender and advanced maternal or paternal age.\u003C\/p\u003E\n         \u003Cp id=\u0022p-6\u0022\u003ELarge-scale genomic studies have yielded a wealth of data on ASD and ID. Novel genome-wide approaches (ie, high resolution arrays using single nucleotide polymorphism [SNP] and copy-number variations [CNV] markers) have identified significantly enriched rare CNVs, including CNVs harboring new susceptibility genes encoding neuronal cell adhesion molecules and ubiquitin pathways [Sanders SJ et al. \u003Cem\u003ENeuron\u003C\/em\u003E 2011; Pinto D et al. \u003Cem\u003ENature\u003C\/em\u003E 2010; Glessner IT et al. \u003Cem\u003ENature\u003C\/em\u003E 2009]. Analysis of the protein-coding portion of the genome with whole exome sequencing (WES) has detected many \u003Cem\u003Ede novo\u003C\/em\u003E and inherited single nucleotide mutations and rare variants in ASD. Using these and other sequencing technologies, genetic mutations have been identified in \u223c20% of ASD cases, but none of the mutations individually accounts for \u0026gt;1% of cases.\u003C\/p\u003E\n         \u003Cp id=\u0022p-7\u0022\u003ESeveral single-gene syndromes are associated with a high rate of patients with ASD symptoms, including Fragile X and Rett syndromes. Many of these disorders are also associated with clinical abnormalities, including dysmorphic features, microcephaly, macrocephaly, and seizures.\u003C\/p\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EIncreased numbers of rare CNVs have been found in individuals with ID, many of which overlap with those found in ASD, epilepsy, schizophrenia, attention deficit disorder, and language impairment, suggesting, at least in part, common abnormalities in early brain development. More than 100 X-linked gene mutations have been associated with single-gene disorders in ID.\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EEvaluation of individuals with ASD and ID using advanced genomic methods can provide a diagnosis and etiology for the disorder, helping to determine prognosis and guide medical care while avoiding unnecessary testing. Genomic testing allows early intervention, counseling, and family planning, providing empowerment and closure to the family. According to the American College of Medical Genetics and Genomics (ACMG), advances in technology have increased the diagnostic yield from 6% to 10% to in the 30% to 40% range [Schaefer GB et al. \u003Cem\u003EGenet Med\u003C\/em\u003E 2013]. The ACMG Practice Guidelines for ASD evaluation are summarized in \u003Ca id=\u0022xref-table-wrap-1-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T1\u0022\u003ETable 1\u003C\/a\u003E. A similar diagnostic strategy is emerging for evaluating ID of unknown etiology, starting with chromosomal microarray (CMA) for first-line genetic testing [Schaefer GB et al. \u003Cem\u003EACMG\u003C\/em\u003E 2013].\u003C\/p\u003E\n         \u003Cdiv id=\u0022T1\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/15905\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/15905\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/15905\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-10\u0022 class=\u0022first-child\u0022\u003EAmerican College of Medical Genetics and Genomics Practice Guidelines for ASD Genetic Evaluation\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-13\u0022\u003EProjected diagnostic yields expected in genetic testing for ASD are shown in \u003Ca id=\u0022xref-table-wrap-2-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T2\u0022\u003ETable 2\u003C\/a\u003E [Schaefer GB et al. \u003Cem\u003EACMG\u003C\/em\u003E 2013].\u003C\/p\u003E\n         \u003Cdiv id=\u0022T2\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/15907\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/15907\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/15907\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 2.\u003C\/span\u003E \n               \u003Cp id=\u0022p-14\u0022 class=\u0022first-child\u0022\u003EProjected Diagnostic Yields in Genetic Evaluation of ASD\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-16\u0022\u003EThe clinical goals of ASD and ID evaluation are to provide affected individuals with tools to achieve their best potential and to provide the best care for the families. Further research on the phenotypic characteristics and their underlying biological mechanisms is needed to develop therapies based on the key vulnerabilities of the pathological mechanisms.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ETARGETING GENE CLUSTERS IN ASD AND ID\u003C\/h2\u003E\n         \u003Cp id=\u0022p-17\u0022\u003EDeveloping potential treatments for ASD and ID is a challenge due to the difficulty in defining clinical phenotypes, severity of the disorders, and the presence of comorbid conditions that can affect the response to treatment, according to Dr. Bolduc. Although there is significant phenotypic and genetic overlap between the 2 disorders, ASD is characterized primarily by restricted behavior and deficits in social communication, while ID is characterized by deficits in intellectual and adaptive functions. In fact, 50% to 85% of ASD patients have ID and 40% of ID patients have ASD [Brereton AV et al. \u003Cem\u003EAutism Dev Disord\u003C\/em\u003E 2006; Matson JL, Shoemaker M. \u003Cem\u003ERes Dev Disabil\u003C\/em\u003E 2009]. Additionally, 20% of novel ASD genes identified with exome sequencing were Fragile X targets [Darnell JC et al. \u003Cem\u003ECell\u003C\/em\u003E 2011].\u003C\/p\u003E\n         \u003Cp id=\u0022p-18\u0022\u003EThe overlapping nature of biological pathways in these disorders suggests that the genes could potentially be clustered into groups to be then targeted by similar drug therapy. Among other ways, ASD and ID genes can be grouped according to their biological function\u2014control of gene expression; regulation of protein synthesis; structural modification of the synapse and neuron; and functional modification of the synapse and neuron. \u003Ca id=\u0022xref-table-wrap-3-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T3\u0022\u003ETable 3\u003C\/a\u003E lists the genes and proteins in each of these pathways that are associated with ASD, ID, and related disorders. A summary of therapies targeting these pathways is also included in the table.\u003C\/p\u003E\n         \u003Cdiv id=\u0022T3\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/15909\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/15909\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/15909\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 3.\u003C\/span\u003E \n               \u003Cp id=\u0022p-19\u0022 class=\u0022first-child\u0022\u003ESummary of Gene Clusters and Targeted Treatments for ASD and ID\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-21\u0022\u003ELarge-scale genetic studies have shown that ASD and ID may have overlapping phenotypic and genetic features. ASD and ID genes may express different phenotypes if they are expressed in different cortical regions [Parishak. \u003Cem\u003ECell\u003C\/em\u003E 2013; Willsey AJ et al. \u003Cem\u003ECell\u003C\/em\u003E 2013]. Clustering ASD and ID genes by function into networks helps in understanding the disorders and in developing treatments targeting these genes. Dr. Bolduc presented a list of multiple online resources that can help clinicians and researchers stay up-to-date on these genetic disorders and related clinical trials: clinical description, \u003Ca href=\u0022http:\/\/OMIM.org\u0022\u003EOMIM.org\u003C\/a\u003E; gene function, \u003Ca href=\u0022http:\/\/geneontology.org\u0022\u003Egeneontology.org\u003C\/a\u003E; where to test, \u003Ca href=\u0022http:\/\/Genetests.org\u0022\u003EGenetests.org\u003C\/a\u003E; and treatments, \u003Ca href=\u0022http:\/\/ClinicalTrials.gov\u0022\u003EClinicalTrials.gov\u003C\/a\u003E.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2014 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/14\/6\/21.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzpac3\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_tables.js?nzpac3\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}