Altered Primary Somatosensory Neuron Development in a Pten Heterozygous Model for Autism Spectrum Disorder / Alejandra FERNANDEZ in Autism Research, 18-11 (November 2025)  

Public ISBD [article]  inAutism Research > 18-11 (November 2025) . - p.2192-2209 Titre : Altered Primary Somatosensory Neuron Development in a Pten Heterozygous Model for Autism Spectrum Disorder Type de document : texte imprimé Auteurs : Alejandra FERNANDEZ, Auteur ; Nick SARN, Auteur ; Charis ENG, Auteur ; Kevin M. WRIGHT, Auteur Article en page(s) : p.2192-2209 Langues : Anglais (eng) Mots-clés : autism Spectrum disorder  DRG  neuronal differentiation  PTEN  somatosensory Index. décimale : PER Périodiques Résumé : ABSTRACT Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by deficits in social interactions, repetitive behaviors, and hyper- or hyposensitivity to sensory stimuli. The cellular mechanisms underlying the emergence of abnormal sensory sensitivity in ASD are not fully understood. Recent studies in rodent models of ASD identified differences in dorsal root ganglia (DRG) neurons that convey somatosensory information to the central nervous system. However, it is unknown how ASD-associated alterations in DRG neurons emerge during development and if these phenotypes are conserved across ASD models. We examined Pten (phosphatase and tensin homolog) heterozygous mice (Pten Het ) as a model for syndromic ASD and identified altered responses to sensory stimuli. Transcriptomic and in vivo analysis identified alterations in subtype-specific markers of DRG neurons in Pten Het mice, emerging during early DRG development and involving dysregulation of signaling pathways downstream of PTEN. Finally, we show that mice harboring an ASD-associated mutation (Pten Y69H ) show nearly identical alterations in the expression of somatosensory neuron subtype-specific markers. These results show that precise levels of PTEN are required for proper somatosensory development and provide insight into the molecular and cellular basis of sensory abnormalities in a model for syndromic ASD. En ligne : https://doi.org/10.1002/aur.70119 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=571 [article] Altered Primary Somatosensory Neuron Development in a Pten Heterozygous Model for Autism Spectrum Disorder [texte imprimé] / Alejandra FERNANDEZ, Auteur ; Nick SARN, Auteur ; Charis ENG, Auteur ; Kevin M. WRIGHT, Auteur . - p.2192-2209. Langues : Anglais (eng) in Autism Research > 18-11 (November 2025) . - p.2192-2209 Mots-clés : autism Spectrum disorder  DRG  neuronal differentiation  PTEN  somatosensory Index. décimale : PER Périodiques Résumé : ABSTRACT Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by deficits in social interactions, repetitive behaviors, and hyper- or hyposensitivity to sensory stimuli. The cellular mechanisms underlying the emergence of abnormal sensory sensitivity in ASD are not fully understood. Recent studies in rodent models of ASD identified differences in dorsal root ganglia (DRG) neurons that convey somatosensory information to the central nervous system. However, it is unknown how ASD-associated alterations in DRG neurons emerge during development and if these phenotypes are conserved across ASD models. We examined Pten (phosphatase and tensin homolog) heterozygous mice (Pten Het ) as a model for syndromic ASD and identified altered responses to sensory stimuli. Transcriptomic and in vivo analysis identified alterations in subtype-specific markers of DRG neurons in Pten Het mice, emerging during early DRG development and involving dysregulation of signaling pathways downstream of PTEN. Finally, we show that mice harboring an ASD-associated mutation (Pten Y69H ) show nearly identical alterations in the expression of somatosensory neuron subtype-specific markers. These results show that precise levels of PTEN are required for proper somatosensory development and provide insight into the molecular and cellular basis of sensory abnormalities in a model for syndromic ASD. En ligne : https://doi.org/10.1002/aur.70119 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=571

Brief Report: Role of Parent-Reported Executive Functioning and Anxiety in Insistence on Sameness in Individuals with Germline PTEN Mutations / Mirko ULJAREVIĆ in Journal of Autism and Developmental Disorders, 52-1 (January 2022)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 52-1 (January 2022) . - p.414-422 Titre : Brief Report: Role of Parent-Reported Executive Functioning and Anxiety in Insistence on Sameness in Individuals with Germline PTEN Mutations Type de document : texte imprimé Auteurs : Mirko ULJAREVIĆ, Auteur ; Thomas W. FRAZIER, Auteur ; Gaëlle RACHED, Auteur ; Robyn M. BUSCH, Auteur ; Patricia KLAAS, Auteur ; Siddharth SRIVASTAVA, Auteur ; Julian A. MARTINEZ-AGOSTO, Auteur ; Mustafa SAHIN, Auteur ; Charis ENG, Auteur ; Antonio Y. HARDAN, Auteur Article en page(s) : p.414-422 Langues : Anglais (eng) Mots-clés : Anxiety/genetics  Autism Spectrum Disorder/genetics  Child  Child, Preschool  Germ Cells  Germ-Line Mutation  Humans  PTEN Phosphohydrolase/genetics  Parents  Anxiety  Executive functioning  Insistence on sameness  Macrocephaly  Pten Index. décimale : PER Périodiques Résumé : This study aimed to characterize the relationship between insistence on sameness (IS), executive functioning (EF) and anxiety among individuals with PTEN mutations and individuals with macrocephalic ASD. The sample included 38 individuals with PTEN mutation and ASD diagnosis (PTEN-ASD; M(age) = 8.93 years, SD(age) = 4.75), 23 with PTEN mutation without ASD (PTEN-no ASD; M(age) = 8.94 years; SD(age) = 4.85) and 25 with ASD and macrocephaly but with no PTEN mutation (Macro-ASD; M(age) = 11.99 years; SD(age) = 5.15). The final model accounted for 45.7% of variance in IS, with Set-Shifting EF subdomain as a unique independent predictor (t = 4.12, p < 0.001). This investigation provides the first preliminary evidence for the EF-anxiety-IS interrelationship in individuals with PTEN mutations and with macrocephalic ASD. En ligne : http://dx.doi.org/10.1007/s10803-021-04881-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=455 [article] Brief Report: Role of Parent-Reported Executive Functioning and Anxiety in Insistence on Sameness in Individuals with Germline PTEN Mutations [texte imprimé] / Mirko ULJAREVIĆ, Auteur ; Thomas W. FRAZIER, Auteur ; Gaëlle RACHED, Auteur ; Robyn M. BUSCH, Auteur ; Patricia KLAAS, Auteur ; Siddharth SRIVASTAVA, Auteur ; Julian A. MARTINEZ-AGOSTO, Auteur ; Mustafa SAHIN, Auteur ; Charis ENG, Auteur ; Antonio Y. HARDAN, Auteur . - p.414-422. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 52-1 (January 2022) . - p.414-422 Mots-clés : Anxiety/genetics  Autism Spectrum Disorder/genetics  Child  Child, Preschool  Germ Cells  Germ-Line Mutation  Humans  PTEN Phosphohydrolase/genetics  Parents  Anxiety  Executive functioning  Insistence on sameness  Macrocephaly  Pten Index. décimale : PER Périodiques Résumé : This study aimed to characterize the relationship between insistence on sameness (IS), executive functioning (EF) and anxiety among individuals with PTEN mutations and individuals with macrocephalic ASD. The sample included 38 individuals with PTEN mutation and ASD diagnosis (PTEN-ASD; M(age) = 8.93 years, SD(age) = 4.75), 23 with PTEN mutation without ASD (PTEN-no ASD; M(age) = 8.94 years; SD(age) = 4.85) and 25 with ASD and macrocephaly but with no PTEN mutation (Macro-ASD; M(age) = 11.99 years; SD(age) = 5.15). The final model accounted for 45.7% of variance in IS, with Set-Shifting EF subdomain as a unique independent predictor (t = 4.12, p < 0.001). This investigation provides the first preliminary evidence for the EF-anxiety-IS interrelationship in individuals with PTEN mutations and with macrocephalic ASD. En ligne : http://dx.doi.org/10.1007/s10803-021-04881-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=455

Cross-level analysis of molecular and neurobehavioral function in a prospective series of patients with germline heterozygous PTEN mutations with and without autism / Thomas W. FRAZIER in Molecular Autism, 12 (2021)  

Public ISBD [article]  inMolecular Autism > 12 (2021) . - 5p. Titre : Cross-level analysis of molecular and neurobehavioral function in a prospective series of patients with germline heterozygous PTEN mutations with and without autism Type de document : texte imprimé Auteurs : Thomas W. FRAZIER, Auteur ; Ritika JAINI, Auteur ; Robyn M. BUSCH, Auteur ; Matthew WOLF, Auteur ; Tammy SADLER, Auteur ; Patricia KLAAS, Auteur ; Antonio Y. HARDAN, Auteur ; Julian A. MARTINEZ-AGOSTO, Auteur ; Mustafa SAHIN, Auteur ; Charis ENG, Auteur Article en page(s) : 5p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder  Behavior  Cognition  Molecular  Pten  Protein Index. décimale : PER Périodiques Résumé : BACKGROUND: PTEN is a well-established risk gene for autism spectrum disorder (ASD). Yet, little is known about how PTEN mutations and associated molecular processes influence neurobehavioral function in mutation carriers with (PTEN-ASD) and without ASD (PTEN no-ASD). The primary aim of the present study was to examine group differences in peripheral blood-derived PTEN pathway protein levels between PTEN-ASD, PTEN no-ASD, and idiopathic macrocephalic ASD patients (macro-ASD). Secondarily, associations between protein levels and neurobehavioral functions were examined in the full cohort. METHODS: Patients were recruited at four tertiary medical centers. Peripheral blood-derived protein levels from canonical PTEN pathways (PI3K/AKT and MAPK/ERK) were analyzed using Western blot analyses blinded to genotype and ASD status. Neurobehavioral measures included standardized assessments of global cognitive ability and multiple neurobehavioral domains. Analysis of variance models examined group differences in demographic, neurobehavioral, and protein measures. Bivariate correlations, structural models, and statistical learning procedures estimated associations between molecular and neurobehavioral variables. To complement patient data, Western blots for downstream proteins were generated to evaluate canonical PTEN pathways in the PTEN-m3m4 mouse model. RESULTS: Participants included 61 patients (25 PTEN-ASD, 16 PTEN no-ASD, and 20 macro-ASD). Decreased PTEN and S6 were observed in both PTEN mutation groups. Reductions in MnSOD and increases in P-S6 were observed in ASD groups. Elevated neural P-AKT/AKT and P-S6/S6 from PTEN murine models parallel our patient observations. Patient PTEN and AKT levels were independently associated with global cognitive ability, and p27 expression was associated with frontal sub-cortical functions. As a group, molecular measures added significant predictive value to several neurobehavioral domains over and above PTEN mutation status. LIMITATIONS: Sample sizes were small, precluding within-group analyses. Protein and neurobehavioral data were limited to a single evaluation. A small number of patients were excluded with invalid protein data, and cognitively impaired patients had missing data on some assessments. CONCLUSIONS: Several canonical PTEN pathway molecules appear to influence the presence of ASD and modify neurobehavioral function in PTEN mutation patients. Protein assays of the PTEN pathway may be useful for predicting neurobehavioral outcomes in PTEN patients. Future longitudinal analyses are needed to replicate these findings and evaluate within-group relationships between protein and neurobehavioral measures. TRIAL REGISTRATION: ClinicalTrials.gov Identifier NCT02461446. En ligne : http://dx.doi.org/10.1186/s13229-020-00406-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=442 [article] Cross-level analysis of molecular and neurobehavioral function in a prospective series of patients with germline heterozygous PTEN mutations with and without autism [texte imprimé] / Thomas W. FRAZIER, Auteur ; Ritika JAINI, Auteur ; Robyn M. BUSCH, Auteur ; Matthew WOLF, Auteur ; Tammy SADLER, Auteur ; Patricia KLAAS, Auteur ; Antonio Y. HARDAN, Auteur ; Julian A. MARTINEZ-AGOSTO, Auteur ; Mustafa SAHIN, Auteur ; Charis ENG, Auteur . - 5p. Langues : Anglais (eng) in Molecular Autism > 12 (2021) . - 5p. Mots-clés : Autism spectrum disorder  Behavior  Cognition  Molecular  Pten  Protein Index. décimale : PER Périodiques Résumé : BACKGROUND: PTEN is a well-established risk gene for autism spectrum disorder (ASD). Yet, little is known about how PTEN mutations and associated molecular processes influence neurobehavioral function in mutation carriers with (PTEN-ASD) and without ASD (PTEN no-ASD). The primary aim of the present study was to examine group differences in peripheral blood-derived PTEN pathway protein levels between PTEN-ASD, PTEN no-ASD, and idiopathic macrocephalic ASD patients (macro-ASD). Secondarily, associations between protein levels and neurobehavioral functions were examined in the full cohort. METHODS: Patients were recruited at four tertiary medical centers. Peripheral blood-derived protein levels from canonical PTEN pathways (PI3K/AKT and MAPK/ERK) were analyzed using Western blot analyses blinded to genotype and ASD status. Neurobehavioral measures included standardized assessments of global cognitive ability and multiple neurobehavioral domains. Analysis of variance models examined group differences in demographic, neurobehavioral, and protein measures. Bivariate correlations, structural models, and statistical learning procedures estimated associations between molecular and neurobehavioral variables. To complement patient data, Western blots for downstream proteins were generated to evaluate canonical PTEN pathways in the PTEN-m3m4 mouse model. RESULTS: Participants included 61 patients (25 PTEN-ASD, 16 PTEN no-ASD, and 20 macro-ASD). Decreased PTEN and S6 were observed in both PTEN mutation groups. Reductions in MnSOD and increases in P-S6 were observed in ASD groups. Elevated neural P-AKT/AKT and P-S6/S6 from PTEN murine models parallel our patient observations. Patient PTEN and AKT levels were independently associated with global cognitive ability, and p27 expression was associated with frontal sub-cortical functions. As a group, molecular measures added significant predictive value to several neurobehavioral domains over and above PTEN mutation status. LIMITATIONS: Sample sizes were small, precluding within-group analyses. Protein and neurobehavioral data were limited to a single evaluation. A small number of patients were excluded with invalid protein data, and cognitively impaired patients had missing data on some assessments. CONCLUSIONS: Several canonical PTEN pathway molecules appear to influence the presence of ASD and modify neurobehavioral function in PTEN mutation patients. Protein assays of the PTEN pathway may be useful for predicting neurobehavioral outcomes in PTEN patients. Future longitudinal analyses are needed to replicate these findings and evaluate within-group relationships between protein and neurobehavioral measures. TRIAL REGISTRATION: ClinicalTrials.gov Identifier NCT02461446. En ligne : http://dx.doi.org/10.1186/s13229-020-00406-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=442

Cytoplasm-predominant Pten associates with increased region-specific brain tyrosine hydroxylase and dopamine D2 receptors in mouse model with autistic traits / Xin HE in Molecular Autism, (November 2015)  

Public ISBD [article]  inMolecular Autism > (November 2015) . - p.1-10 Titre : Cytoplasm-predominant Pten associates with increased region-specific brain tyrosine hydroxylase and dopamine D2 receptors in mouse model with autistic traits Type de document : texte imprimé Auteurs : Xin HE, Auteur ; Stetson THACKER, Auteur ; Todd ROMIGH, Auteur ; Qi YU, Auteur ; Thomas W. FRAZIER, Auteur ; Charis ENG, Auteur Article en page(s) : p.1-10 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by impairment in social communication/interaction and inflexible/repetitive behavior. Several lines of evidence support genetic factors as a predominant cause of ASD. Among those autism susceptibility genes that have been identified, the PTEN tumor suppressor gene, initially identified as predisposing to Cowden heritable cancer syndrome, was found to be mutated in a subset of ASD patients with extreme macrocephaly. However, the ASD-relevant molecular mechanism mediating the effect of PTEN mutations remains elusive. En ligne : http://dx.doi.org/10.1186/s13229-015-0056-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277 [article] Cytoplasm-predominant Pten associates with increased region-specific brain tyrosine hydroxylase and dopamine D2 receptors in mouse model with autistic traits [texte imprimé] / Xin HE, Auteur ; Stetson THACKER, Auteur ; Todd ROMIGH, Auteur ; Qi YU, Auteur ; Thomas W. FRAZIER, Auteur ; Charis ENG, Auteur . - p.1-10. Langues : Anglais (eng) in Molecular Autism > (November 2015) . - p.1-10 Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by impairment in social communication/interaction and inflexible/repetitive behavior. Several lines of evidence support genetic factors as a predominant cause of ASD. Among those autism susceptibility genes that have been identified, the PTEN tumor suppressor gene, initially identified as predisposing to Cowden heritable cancer syndrome, was found to be mutated in a subset of ASD patients with extreme macrocephaly. However, the ASD-relevant molecular mechanism mediating the effect of PTEN mutations remains elusive. En ligne : http://dx.doi.org/10.1186/s13229-015-0056-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277

Decreased nuclear Pten in neural stem cells contributes to deficits in neuronal maturation / Shin Chung KANG in Molecular Autism, 11 (2020)  

Public ISBD [article]  inMolecular Autism > 11 (2020) . - 43 p. Titre : Decreased nuclear Pten in neural stem cells contributes to deficits in neuronal maturation Type de document : texte imprimé Auteurs : Shin Chung KANG, Auteur ; Ritika JAINI, Auteur ; Masahiro HITOMI, Auteur ; Hyunpil LEE, Auteur ; Nick SARN, Auteur ; Stetson THACKER, Auteur ; Charis ENG, Auteur Article en page(s) : 43 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder  Creb activation  Neural development  Neural stem cells  Neuronal maturation  PTEN mutation Index. décimale : PER Périodiques Résumé : BACKGROUND: PTEN, a syndromic autism spectrum disorder (ASD) risk gene, is mutated in approximately 10% of macrocephalic ASD cases. Despite the described genetic association between PTEN and ASD and ensuing studies, we continue to have a limited understanding of how PTEN disruption drives ASD pathogenesis and maintenance. METHODS: We derived neural stem cells (NSCs) from the dentate gyrus (DG) of Pten(m3m4) mice, a model that recapitulates PTEN-ASD phenotypes. We subsequently characterized the expression of stemness factors, proliferation, and differentiation of neurons and glia in Pten(m3m4) NSCs using immunofluorescent and immunoblotting approaches. We also measured Creb phosphorylation by Western blot analysis and expression of Creb-regulated genes with qRT-PCR. RESULTS: The m3m4 mutation decreases Pten localization to the nucleus and its global expression over time. Pten(m3m4) NSCs exhibit persistent stemness characteristics associated with increased proliferation and a resistance to neuronal maturation during differentiation. Given the increased proliferation of Pten(m3m4) NSCs, a significant increase in the population of immature neurons relative to mature neurons occurs, an approximately tenfold decrease in the ratio between the homozygous mutant and wildtype. There is an opposite pattern of differentiation in some Pten(m3m4) glia, specifically an increase in astrocytes. These aberrant differentiation patterns associate with changes in Creb activation in Pten(m3m4/m3m4) NSCs. We specifically observed loss of Creb phosphorylation at S133 in Pten(m3m4/m3m4) NSCs and a subsequent decrease in expression of Creb-regulated genes important to neuronal function (i.e., Bdnf). Interestingly, Bdnf treatment is able to partially rescue the stunted neuronal maturation phenotype in Pten(m3m4/m3m4) NSCs. CONCLUSIONS: Constitutional disruption of Pten nuclear localization with subsequent global decrease in Pten expression generates abnormal patterns of differentiation, a stunting of neuronal maturation. The propensity of Pten disruption to restrain neurons to a more progenitor-like state may be an important feature contributing to PTEN-ASD pathogenesis. En ligne : http://dx.doi.org/10.1186/s13229-020-00337-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427 [article] Decreased nuclear Pten in neural stem cells contributes to deficits in neuronal maturation [texte imprimé] / Shin Chung KANG, Auteur ; Ritika JAINI, Auteur ; Masahiro HITOMI, Auteur ; Hyunpil LEE, Auteur ; Nick SARN, Auteur ; Stetson THACKER, Auteur ; Charis ENG, Auteur . - 43 p. Langues : Anglais (eng) in Molecular Autism > 11 (2020) . - 43 p. Mots-clés : Autism spectrum disorder  Creb activation  Neural development  Neural stem cells  Neuronal maturation  PTEN mutation Index. décimale : PER Périodiques Résumé : BACKGROUND: PTEN, a syndromic autism spectrum disorder (ASD) risk gene, is mutated in approximately 10% of macrocephalic ASD cases. Despite the described genetic association between PTEN and ASD and ensuing studies, we continue to have a limited understanding of how PTEN disruption drives ASD pathogenesis and maintenance. METHODS: We derived neural stem cells (NSCs) from the dentate gyrus (DG) of Pten(m3m4) mice, a model that recapitulates PTEN-ASD phenotypes. We subsequently characterized the expression of stemness factors, proliferation, and differentiation of neurons and glia in Pten(m3m4) NSCs using immunofluorescent and immunoblotting approaches. We also measured Creb phosphorylation by Western blot analysis and expression of Creb-regulated genes with qRT-PCR. RESULTS: The m3m4 mutation decreases Pten localization to the nucleus and its global expression over time. Pten(m3m4) NSCs exhibit persistent stemness characteristics associated with increased proliferation and a resistance to neuronal maturation during differentiation. Given the increased proliferation of Pten(m3m4) NSCs, a significant increase in the population of immature neurons relative to mature neurons occurs, an approximately tenfold decrease in the ratio between the homozygous mutant and wildtype. There is an opposite pattern of differentiation in some Pten(m3m4) glia, specifically an increase in astrocytes. These aberrant differentiation patterns associate with changes in Creb activation in Pten(m3m4/m3m4) NSCs. We specifically observed loss of Creb phosphorylation at S133 in Pten(m3m4/m3m4) NSCs and a subsequent decrease in expression of Creb-regulated genes important to neuronal function (i.e., Bdnf). Interestingly, Bdnf treatment is able to partially rescue the stunted neuronal maturation phenotype in Pten(m3m4/m3m4) NSCs. CONCLUSIONS: Constitutional disruption of Pten nuclear localization with subsequent global decrease in Pten expression generates abnormal patterns of differentiation, a stunting of neuronal maturation. The propensity of Pten disruption to restrain neurons to a more progenitor-like state may be an important feature contributing to PTEN-ASD pathogenesis. En ligne : http://dx.doi.org/10.1186/s13229-020-00337-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427

Demographic and clinical correlates of autism symptom domains and autism spectrum diagnosis / Thomas W. FRAZIER in Autism, 18-5 (July 2014)  

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Erratum to: Cytoplasm-predominant Pten associates with increased region-specific brain tyrosine hydroxylase and dopamine D2 receptors in mouse model with autistic traits / Xin HE in Molecular Autism, 7 (2016)  

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Germline nuclear-predominant Pten murine model exhibits impaired social and perseverative behavior, microglial activation, and increased oxytocinergic activity / Nick SARN in Molecular Autism, 12 (2021)  

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Longitudinal neurobehavioral profiles in children and young adults with PTEN hamartoma tumor syndrome and reliable methods for assessing neurobehavioral change / Robyn M. BUSCH in Journal of Neurodevelopmental Disorders, 15 (2023)  

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Quantitative autism symptom patterns recapitulate differential mechanisms of genetic transmission in single and multiple incidence families / Thomas W. FRAZIER in Molecular Autism, (October 2015)  

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Remote monitoring of social attention in neurogenetic syndromes and idiopathic neurodevelopmental disability / Thomas W. FRAZIER ; Robyn M. BUSCH ; Patricia KLAAS ; Katherine LACHLAN ; Shafali S. JESTE ; Alexander KOLEVZON ; Eva LOTH ; Jacqueline HARRIS ; Tom PEPPER ; Kristin ANTHONY ; J. Michael GRAGLIA ; Kathryn HELDE ; Christal DELAGRAMMATIKAS ; Sandra BEDROSIAN-SERMONE ; Constance SMITH-HICKS ; Mustafa SAHIN ; Eric A. YOUNGSTROM ; Charis ENG ; Lacey CHETCUTI ; Antonio Y. HARDAN ; Mirko ULJAREVIĆ in Autism Research, 18-2 (February 2025)  

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A Twin Study of Heritable and Shared Environmental Contributions to Autism / Thomas W. FRAZIER in Journal of Autism and Developmental Disorders, 44-8 (August 2014)  

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