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Auteur Joseph D. BUXBAUM |
Documents disponibles écrits par cet auteur (67)
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[article]
Titre : Advancing paternal age and simplex autism Type de document : Texte imprimé et/ou numérique Auteurs : Connor M. PULEO, Auteur ; James SCHMEIDLER, Auteur ; Abraham REICHENBERG, Auteur ; Alexander KOLEVZON, Auteur ; Latha V. SOORYA, Auteur ; Joseph D. BUXBAUM, Auteur Année de publication : 2012 Article en page(s) : p.367-380 Langues : Anglais (eng) Mots-clés : autism spectrum disorder de novo multiplex paternal age sex differences simplex Index. décimale : PER Périodiques Résumé : De novo events appear more common in female and simplex autism spectrum disorder (ASD) cases and may underlie greater ASD risk in older fathers’ offspring. This study examined whether advancing paternal age predicts an increase in simplex (n = 90) versus multiplex ASD cases (n = 587) in 677 participants (340 families). Whether or not controlling for maternal age, results support a significant interaction of linear paternal age and sex of the child on simplex family type. Female ASD cases were significantly more likely to be simplex as paternal age increased, but the increase for males was not significant. Findings suggest that ASD arising from non-familial, de novo events may be far less prominent in males than in females, even if more prevalent in males, due to the substantially larger number of male cases attributable to other, more strongly male-biased risk factors. En ligne : http://dx.doi.org/10.1177/1362361311427154 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=178
in Autism > 16-4 (July 2012) . - p.367-380[article] Advancing paternal age and simplex autism [Texte imprimé et/ou numérique] / Connor M. PULEO, Auteur ; James SCHMEIDLER, Auteur ; Abraham REICHENBERG, Auteur ; Alexander KOLEVZON, Auteur ; Latha V. SOORYA, Auteur ; Joseph D. BUXBAUM, Auteur . - 2012 . - p.367-380.
Langues : Anglais (eng)
in Autism > 16-4 (July 2012) . - p.367-380
Mots-clés : autism spectrum disorder de novo multiplex paternal age sex differences simplex Index. décimale : PER Périodiques Résumé : De novo events appear more common in female and simplex autism spectrum disorder (ASD) cases and may underlie greater ASD risk in older fathers’ offspring. This study examined whether advancing paternal age predicts an increase in simplex (n = 90) versus multiplex ASD cases (n = 587) in 677 participants (340 families). Whether or not controlling for maternal age, results support a significant interaction of linear paternal age and sex of the child on simplex family type. Female ASD cases were significantly more likely to be simplex as paternal age increased, but the increase for males was not significant. Findings suggest that ASD arising from non-familial, de novo events may be far less prominent in males than in females, even if more prevalent in males, due to the substantially larger number of male cases attributable to other, more strongly male-biased risk factors. En ligne : http://dx.doi.org/10.1177/1362361311427154 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=178 Altered synaptic ultrastructure in the prefrontal cortex of Shank3-deficient rats / Sarah JACOT-DESCOMBES in Molecular Autism, 11 (2020)
[article]
Titre : Altered synaptic ultrastructure in the prefrontal cortex of Shank3-deficient rats Type de document : Texte imprimé et/ou numérique Auteurs : Sarah JACOT-DESCOMBES, Auteur ; Neha U. KESHAV, Auteur ; Dara L. DICKSTEIN, Auteur ; Bridget WICINSKI, Auteur ; William G. M. JANSSEN, Auteur ; Liam L. HIESTER, Auteur ; Edward K. SARFO, Auteur ; Tahia WARDA, Auteur ; Matthew M. FAM, Auteur ; Hala HARONY-NICOLAS, Auteur ; Joseph D. BUXBAUM, Auteur ; Patrick R. HOF, Auteur ; Merina VARGHESE, Auteur Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Electron microscopy Phelan–McDermid syndrome Synapse morphology Index. décimale : PER Périodiques Résumé : BACKGROUND: Deletion or mutations of SHANK3 lead to Phelan-McDermid syndrome and monogenic forms of autism spectrum disorder (ASD). SHANK3 encodes its eponymous scaffolding protein at excitatory glutamatergic synapses. Altered morphology of dendrites and spines in the hippocampus, cerebellum, and striatum have been associated with behavioral impairments in Shank3-deficient animal models. Given the attentional deficit in these animals, our study explored whether deficiency of Shank3 in a rat model alters neuron morphology and synaptic ultrastructure in the medial prefrontal cortex (mPFC). METHODS: We assessed dendrite and spine morphology and spine density in mPFC layer III neurons in Shank3-homozygous knockout (Shank3-KO), heterozygous (Shank3-Het), and wild-type (WT) rats. We used electron microscopy to determine the density of asymmetric synapses in mPFC layer III excitatory neurons in these rats. We measured postsynaptic density (PSD) length, PSD area, and head diameter (HD) of spines at these synapses. RESULTS: Basal dendritic morphology was similar among the three genotypes. Spine density and morphology were comparable, but more thin and mushroom spines had larger head volumes in Shank3-Het compared to WT and Shank3-KO. All three groups had comparable synapse density and PSD length. Spine HD of total and non-perforated synapses in Shank3-Het rats, but not Shank3-KO rats, was significantly larger than in WT rats. The total and non-perforated PSD area was significantly larger in Shank3-Het rats compared to Shank3-KO rats. These findings represent preliminary evidence for synaptic ultrastructural alterations in the mPFC of rats that lack one copy of Shank3 and mimic the heterozygous loss of SHANK3 in Phelan-McDermid syndrome. LIMITATIONS: The Shank3 deletion in the rat model we used does not affect all isoforms of the protein and would only model the effect of mutations resulting in loss of the N-terminus of the protein. Given the higher prevalence of ASD in males, the ultrastructural study focused only on synaptic structure in male Shank3-deficient rats. CONCLUSIONS: We observed increased HD and PSD area in Shank3-Het rats. These observations suggest the occurrence of altered synaptic ultrastructure in this animal model, further pointing to a key role of defective expression of the Shank3 protein in ASD and Phelan-McDermid syndrome. En ligne : http://dx.doi.org/10.1186/s13229-020-00393-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438
in Molecular Autism > 11 (2020)[article] Altered synaptic ultrastructure in the prefrontal cortex of Shank3-deficient rats [Texte imprimé et/ou numérique] / Sarah JACOT-DESCOMBES, Auteur ; Neha U. KESHAV, Auteur ; Dara L. DICKSTEIN, Auteur ; Bridget WICINSKI, Auteur ; William G. M. JANSSEN, Auteur ; Liam L. HIESTER, Auteur ; Edward K. SARFO, Auteur ; Tahia WARDA, Auteur ; Matthew M. FAM, Auteur ; Hala HARONY-NICOLAS, Auteur ; Joseph D. BUXBAUM, Auteur ; Patrick R. HOF, Auteur ; Merina VARGHESE, Auteur.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020)
Mots-clés : Autism spectrum disorder Electron microscopy Phelan–McDermid syndrome Synapse morphology Index. décimale : PER Périodiques Résumé : BACKGROUND: Deletion or mutations of SHANK3 lead to Phelan-McDermid syndrome and monogenic forms of autism spectrum disorder (ASD). SHANK3 encodes its eponymous scaffolding protein at excitatory glutamatergic synapses. Altered morphology of dendrites and spines in the hippocampus, cerebellum, and striatum have been associated with behavioral impairments in Shank3-deficient animal models. Given the attentional deficit in these animals, our study explored whether deficiency of Shank3 in a rat model alters neuron morphology and synaptic ultrastructure in the medial prefrontal cortex (mPFC). METHODS: We assessed dendrite and spine morphology and spine density in mPFC layer III neurons in Shank3-homozygous knockout (Shank3-KO), heterozygous (Shank3-Het), and wild-type (WT) rats. We used electron microscopy to determine the density of asymmetric synapses in mPFC layer III excitatory neurons in these rats. We measured postsynaptic density (PSD) length, PSD area, and head diameter (HD) of spines at these synapses. RESULTS: Basal dendritic morphology was similar among the three genotypes. Spine density and morphology were comparable, but more thin and mushroom spines had larger head volumes in Shank3-Het compared to WT and Shank3-KO. All three groups had comparable synapse density and PSD length. Spine HD of total and non-perforated synapses in Shank3-Het rats, but not Shank3-KO rats, was significantly larger than in WT rats. The total and non-perforated PSD area was significantly larger in Shank3-Het rats compared to Shank3-KO rats. These findings represent preliminary evidence for synaptic ultrastructural alterations in the mPFC of rats that lack one copy of Shank3 and mimic the heterozygous loss of SHANK3 in Phelan-McDermid syndrome. LIMITATIONS: The Shank3 deletion in the rat model we used does not affect all isoforms of the protein and would only model the effect of mutations resulting in loss of the N-terminus of the protein. Given the higher prevalence of ASD in males, the ultrastructural study focused only on synaptic structure in male Shank3-deficient rats. CONCLUSIONS: We observed increased HD and PSD area in Shank3-Het rats. These observations suggest the occurrence of altered synaptic ultrastructure in this animal model, further pointing to a key role of defective expression of the Shank3 protein in ASD and Phelan-McDermid syndrome. En ligne : http://dx.doi.org/10.1186/s13229-020-00393-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438 Altered tactile processing in children with autism spectrum disorder / Teresa TAVASSOLI in Autism Research, 9-6 (June 2016)
[article]
Titre : Altered tactile processing in children with autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Teresa TAVASSOLI, Auteur ; Katherine BELLESHEIM, Auteur ; Mark TOMMERDAHL, Auteur ; Jameson M. HOLDEN, Auteur ; Alexander KOLEVZON, Auteur ; Joseph D. BUXBAUM, Auteur Article en page(s) : p.616-620 Langues : Anglais (eng) Mots-clés : tactile processing inhibition autism spectrum disorder GABA Index. décimale : PER Périodiques Résumé : Although tactile reactivity issues are commonly reported in children with autism spectrum disorder (ASD), the underlying mechanisms are poorly understood. Less feed-forward inhibition has been proposed as a potential mechanism for some symptoms of ASD. We tested static and dynamic tactile thresholds as a behavioral proxy of feed-forward inhibition in 42 children (21 children with ASD and 21 typically developing [TD] children). Subthreshold conditioning typically raises the dynamic detection threshold, thus comparison of the dynamic to the static threshold generates a metric that predicts gamma-aminobutyric acid (GABA) mediated feed-forward inhibition. Children with ASD had marginally higher static thresholds and a significantly lower ratio between thresholds as compared with TD children. The lower ratio, only seen in children with ASD, might be indicative of less inhibition. Static thresholds were correlated with autism spectrum quotient scores, indicating the higher the tactile threshold, the more ASD traits. The amount of feed-forward inhibition (ratio between dynamic/static) was negatively correlated with autism diagnostic observation schedule repetitive behavior scores, meaning the less inhibition the more ASD symptoms. In summary, children with ASD showed altered tactile processing compared with TD children; thus measuring static and dynamic thresholds could be a potential biomarker for ASD and might be useful for prediction of treatment response with therapeutics, including those that target the GABAergic system. Autism Res 2016, 9: 616–620. © 2015 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1563 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=290
in Autism Research > 9-6 (June 2016) . - p.616-620[article] Altered tactile processing in children with autism spectrum disorder [Texte imprimé et/ou numérique] / Teresa TAVASSOLI, Auteur ; Katherine BELLESHEIM, Auteur ; Mark TOMMERDAHL, Auteur ; Jameson M. HOLDEN, Auteur ; Alexander KOLEVZON, Auteur ; Joseph D. BUXBAUM, Auteur . - p.616-620.
Langues : Anglais (eng)
in Autism Research > 9-6 (June 2016) . - p.616-620
Mots-clés : tactile processing inhibition autism spectrum disorder GABA Index. décimale : PER Périodiques Résumé : Although tactile reactivity issues are commonly reported in children with autism spectrum disorder (ASD), the underlying mechanisms are poorly understood. Less feed-forward inhibition has been proposed as a potential mechanism for some symptoms of ASD. We tested static and dynamic tactile thresholds as a behavioral proxy of feed-forward inhibition in 42 children (21 children with ASD and 21 typically developing [TD] children). Subthreshold conditioning typically raises the dynamic detection threshold, thus comparison of the dynamic to the static threshold generates a metric that predicts gamma-aminobutyric acid (GABA) mediated feed-forward inhibition. Children with ASD had marginally higher static thresholds and a significantly lower ratio between thresholds as compared with TD children. The lower ratio, only seen in children with ASD, might be indicative of less inhibition. Static thresholds were correlated with autism spectrum quotient scores, indicating the higher the tactile threshold, the more ASD traits. The amount of feed-forward inhibition (ratio between dynamic/static) was negatively correlated with autism diagnostic observation schedule repetitive behavior scores, meaning the less inhibition the more ASD symptoms. In summary, children with ASD showed altered tactile processing compared with TD children; thus measuring static and dynamic thresholds could be a potential biomarker for ASD and might be useful for prediction of treatment response with therapeutics, including those that target the GABAergic system. Autism Res 2016, 9: 616–620. © 2015 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1563 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=290 An overview of the genetics of autism spectrum disorders / Joseph D. BUXBAUM
Titre : An overview of the genetics of autism spectrum disorders Type de document : Texte imprimé et/ou numérique Auteurs : Joseph D. BUXBAUM, Auteur Année de publication : 2013 Importance : p.46-56 Langues : Anglais (eng) Index. décimale : SCI-D SCI-D - Neurosciences Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189 An overview of the genetics of autism spectrum disorders [Texte imprimé et/ou numérique] / Joseph D. BUXBAUM, Auteur . - 2013 . - p.46-56.
Langues : Anglais (eng)
Index. décimale : SCI-D SCI-D - Neurosciences Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189 Exemplaires
Code-barres Cote Support Localisation Section Disponibilité aucun exemplaire Animal Models for Neurodevelopmental Disorders / Hala HARONY-NICOLAS
Titre : Animal Models for Neurodevelopmental Disorders Type de document : Texte imprimé et/ou numérique Auteurs : Hala HARONY-NICOLAS, Auteur ; Joseph D. BUXBAUM, Auteur Année de publication : 2015 Importance : p.261-274 Langues : Anglais (eng) Index. décimale : SCI-B SCI-B - Génétique Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=400 Animal Models for Neurodevelopmental Disorders [Texte imprimé et/ou numérique] / Hala HARONY-NICOLAS, Auteur ; Joseph D. BUXBAUM, Auteur . - 2015 . - p.261-274.
Langues : Anglais (eng)
Index. décimale : SCI-B SCI-B - Génétique Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=400 Exemplaires
Code-barres Cote Support Localisation Section Disponibilité aucun exemplaire Assessing the utility of electronic measures as a proxy for cognitive ability / Tess LEVY in Autism Research, 15-6 (June 2022)
PermalinkBrief Report: Assessment of a Caregiver-Implemented Intervention for Improving Social Communication Skills in Toddlers and Young Children with Autism / Christine HONSBERGER ; Nathaniel A. SHANOK ; Erin Brooker LOZOTT ; Tess LEVY ; Alexander KOLEVZON ; Joseph D. BUXBAUM ; Marlene SOTELO ; Jennifer FOSS-FEIG ; Paige M. SIPER in Journal of Autism and Developmental Disorders, 54-2 (February 2024)
PermalinkBrief Report: The Autism Mental Status Examination: Development of a Brief Autism-Focused Exam / David GRODBERG in Journal of Autism and Developmental Disorders, 42-3 (March 2012)
PermalinkCandidate susceptibility genes for autism / Irina N. BESPALOVA
PermalinkCapping four years of growth of Molecular Autism: impact factor coming in 2014 / Joseph D. BUXBAUM in Molecular Autism, (December 2013)
PermalinkA clinician-administered observation and corresponding caregiver interview capturing DSM-5 sensory reactivity symptoms in children with ASD / Paige M. SIPER in Autism Research, 10-6 (June 2017)
PermalinkDAWN: a framework to identify autism genes and subnetworks using gene expression and genetics / Li LIU in Molecular Autism, (March 2014)
PermalinkDelineation of the genetic and clinical spectrum of Phelan-McDermid syndrome caused by SHANK3 point mutations / S. DE RUBEIS in Molecular Autism, 9 (2018)
PermalinkDevelopmental social communication deficits in the Shank3 rat model of phelan-mcdermid syndrome and autism spectrum disorder / Elizabeth L. BERG in Autism Research, 11-4 (April 2018)
PermalinkDid Hans Asperger actively assist the Nazi euthanasia program? / Simon BARON-COHEN in Molecular Autism, 9 (2018)
PermalinkPermalinkErratum: A pilot controlled trial of insulin-like growth factor-1 in children with Phelan-McDermid syndrome / Alexander KOLEVZON in Molecular Autism, (June 2015)
PermalinkErratum to: Neural selectivity for communicative auditory signals in Phelan-McDermid syndrome / A. Ting WANG in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)
PermalinkExamining the Efficacy of a Family Peer Advocate Model for Black and Hispanic Caregivers of Children with Autism Spectrum Disorder / J. M. JAMISON in Journal of Autism and Developmental Disorders, 47-5 (May 2017)
PermalinkGenetics in psychiatry: common variant association studies / Joseph D. BUXBAUM in Molecular Autism, (March 2010)
PermalinkGetting from 1,000 Genes to a Triad of Symptoms: The Emerging Role of Systems Biology in Autism Spectrum Disorders / Joseph D. BUXBAUM
PermalinkGrandma knows best: Family structure and age of diagnosis of autism spectrum disorder / N. SICHERMAN in Autism, 22-3 (April 2018)
PermalinkHaploinsufficiency of Gtf2i, a gene deleted in Williams Syndrome, leads to increases in social interactions / Takeshi SAKURAI in Autism Research, 4-1 (February 2011)
PermalinkHaploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication / Ozlem BOZDAGI in Molecular Autism, (December 2010)
PermalinkHow rare and common risk variation jointly affect liability for autism spectrum disorder / L. KLEI in Molecular Autism, 12 (2021)
PermalinkIndividuals with FOXP1 syndrome present with a complex neurobehavioral profile with high rates of ADHD, anxiety, repetitive behaviors, and sensory symptoms / M. P. TRELLES in Molecular Autism, 12 (2021)
PermalinkInsulin-like growth factor-1 rescues synaptic and motor deficits in a mouse model of autism and developmental delay / Ozlem BOZDAGI in Molecular Autism, (April 2013)
PermalinkIntestinal dysmotility in a zebrafish (Danio rerio) shank3a;shank3b mutant model of autism / D. M. JAMES in Molecular Autism, 10 (2019)
PermalinkLanguage ENvironment Analysis (LENA) in Phelan-McDermid Syndrome: Validity and Suggestions for Use in Minimally Verbal Children with Autism Spectrum Disorder / Jacquelin RANKINE in Journal of Autism and Developmental Disorders, 47-6 (June 2017)
PermalinkA large-scale screen for coding variants in SERT/SLC6A4 in autism spectrum disorders / Takeshi SAKURAI in Autism Research, 1-4 (August 2008)
PermalinkA large-scale survey of the novel 15q24 microdeletion syndrome in autism spectrum disorders identifies an atypical deletion that narrows the critical region / L. Alison MCINNES in Molecular Autism, (March 2010)
PermalinkMeasuring Sensory Reactivity in Autism Spectrum Disorder: Application and Simplification of a Clinician-Administered Sensory Observation Scale / Teresa TAVASSOLI in Journal of Autism and Developmental Disorders, 46-1 (January 2016)
PermalinkMolecular Autism: accelerating and integrating research into neurodevelopmental conditions / Joseph D. BUXBAUM in Molecular Autism, (February 2010)
PermalinkNeural selectivity for communicative auditory signals in Phelan-McDermid syndrome / A. Ting WANG in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)
PermalinkNeuropathology of the posteroinferior occipitotemporal gyrus in children with autism / Neha UPPAL in Molecular Autism, (February 2014)
PermalinkNeuropsychiatric decompensation in adolescents and adults with Phelan-McDermid syndrome: a systematic review of the literature / A. KOLEVZON in Molecular Autism, 10 (2019)
PermalinkNext-Generation Sequencing For Gene and Pathway Discovery and Analysis in Autism Spectrum Disorders / Guiqing CAI
PermalinkNo evidence for IL1RAPL1 involvement in selected high-risk autism pedigrees from the AGRE data set / Kristina ALLEN-BRADY in Autism Research, 4-4 (August 2011)
PermalinkOptimizing the phenotyping of rodent ASD models: Enrichment analysis of mouse and human neurobiological phenotypes associated with high-risk autism genes identifies morphological, electrophysiological, neurological, and behavioral features / Joseph D. BUXBAUM in Molecular Autism, (February 2012)
PermalinkPhelan-McDermid syndrome: a review of the literature and practice parameters for medical assessment and monitoring / A. KOLEVZON in Journal of Neurodevelopmental Disorders, 6-1 (December 2014)
PermalinkPhenotypic and functional analysis of SHANK3 stop mutations identified in individuals with ASD and/or ID / Daniela M. COCHOY in Molecular Autism, (April 2015)
PermalinkA pilot controlled trial of insulin-like growth factor-1 in children with Phelan-McDermid syndrome / Alexander KOLEVZON in Molecular Autism, (December 2014)
PermalinkPrevalence and phenotypic impact of rare potentially damaging variants in autism spectrum disorder / B. MAHJANI in Molecular Autism, 12 (2021)
PermalinkA proof-of-concept study of growth hormone in children with Phelan-McDermid syndrome / S. SETHURAM in Molecular Autism, 13 (2022)
PermalinkProspective and detailed behavioral phenotyping in DDX3X syndrome / L. TANG in Molecular Autism, 12 (2021)
PermalinkProspective investigation of autism and genotype-phenotype correlations in 22q13 deletion syndrome and SHANK3 deficiency / Latha V. SOORYA in Molecular Autism, (June 2013)
PermalinkPermalinkPsychometric Study of the Social Responsiveness Scale in Phelan-McDermid Syndrome / Kellie GERGOUDIS in Autism Research, 13-8 (August 2020)
PermalinkA randomized controlled trial of intranasal oxytocin in Phelan-McDermid syndrome / J. FASTMAN in Molecular Autism, 12 (2021)
PermalinkReduced brain volume and white matter alterations in Shank3-deficient rats / C. E. M. GOLDEN in Autism Research, 14-9 (September 2021)
PermalinkReduced engagement of visual attention in children with autism spectrum disorder / C. S. MCLAUGHLIN in Autism, 25-7 (October 2021)
PermalinkReduced engagement of visual attention in children with autism spectrum disorder / Christopher S. MCLAUGHLIN in Autism, 26-7 (October 2022)
PermalinkRigor in science and science reporting: updated guidelines for submissions to Molecular Autism / Joseph D. BUXBAUM in Molecular Autism, 10 (2019)
PermalinkSHANK2 and SHANK3 Mutations Implicate Glutamate Signaling Abnormalities in Autism Spectrum Disorders / Hala HARONY-NICOLAS
PermalinkShank3?deficient rats exhibit degraded cortical responses to sound / T. ENGINEER CRYSTAL in Autism Research, 11-1 (January 2018)
PermalinkSHANK3 haploinsufficiency: a common but underdiagnosed highly penetrant monogenic cause of autism spectrum disorders / Catalina BETANCUR in Molecular Autism, (June 2013)
PermalinkShifted phase of EEG cross-frequency coupling in individuals with Phelan-McDermid syndrome / M. G. MARISCAL in Molecular Autism, 12 (2021)
PermalinkA Simplified Diagnostic Observational Assessment of Autism Spectrum Disorder in Early Childhood / David GRODBERG in Autism Research, 9-4 (April 2016)
PermalinkThe Autism Mental Status Exam: Sensitivity and Specificity Using DSM-5 Criteria for Autism Spectrum Disorder in Verbally Fluent Adults / David GRODBERG in Journal of Autism and Developmental Disorders, 44-3 (March 2014)
PermalinkThe Autism Simplex Collection: an international, expertly phenotyped autism sample for genetic and phenotypic analyses / Joseph D. BUXBAUM in Molecular Autism, (May 2014)
PermalinkThe Effect of an Autism-Associated Polymorphism in the STK39 Gene on the Autism Symptom Domains / Rick D. VAVOLIZZA in Journal of Autism and Developmental Disorders, 42-2 (February 2012)
PermalinkThe Immersive Theater Experience for Individuals with Autism Spectrum Disorder / Ivy GISERMAN-KISS in Journal of Autism and Developmental Disorders, 50-3 (March 2020)
PermalinkThe Neuroscience of Autism Spectrum Disorders / Joseph D. BUXBAUM
PermalinkTranscriptional signatures of participant-derived neural progenitor cells and neurons implicate altered Wnt signaling in Phelan-McDermid syndrome and autism / Michael S. BREEN in Molecular Autism, 11 (2020)
PermalinkTranscriptomic changes in the frontal cortex associated with paternal age / Rebecca G. SMITH in Molecular Autism, (March 2014)
PermalinkUltrastructural analyses in the hippocampus CA1 field in Shank3-deficient mice / Neha UPPAL in Molecular Autism, (June 2015)
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