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Copy-number variants in the contactin-5 gene are a potential risk factor for autism spectrum disorder / Zoe SCHMILOVICH in Research in Autism Spectrum Disorders, 99 (November)
[article]
Titre : Copy-number variants in the contactin-5 gene are a potential risk factor for autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Zoe SCHMILOVICH, Auteur ; Guillaume HUGUET, Auteur ; Qin HE, Auteur ; Amélie MUSA-JOHNSON, Auteur ; Elise DOUARD, Auteur ; Mor Absa LOUM, Auteur ; Calwing LIAO, Auteur ; Jay P. ROSS, Auteur ; Alexandre DIONNE-LAPORTE, Auteur ; Dan SPIEGELMAN, Auteur ; Martineau JEAN-LOUIS, Auteur ; Zohra SACI, Auteur ; Caroline HAYWARD, Auteur ; Tobias BANASCHEWSKI, Auteur ; Arun BOKDE, Auteur ; Sylvane DESRIVIERES, Auteur ; Herve LEMAITRE, Auteur ; Gunter SCHUMANN, Auteur ; Lan XIONG, Auteur ; Patrick A. DION, Auteur ; Sébastien JACQUEMONT, Auteur ; Boris CHAUMETTE, Auteur ; Guy A. ROULEAU, Auteur Article en page(s) : 102055 Langues : Anglais (eng) Mots-clés : CNTN5 CNV intronic deletions neurodevelopment inherited Index. décimale : PER Périodiques Résumé : Background Contactin-5 (CNTN5) is a candidate risk gene for autism spectrum disorder (ASD). Previous attempts to associate CNTN5 CNVs with ASD-susceptibility were limited by insufficient statistical power. Here, we aim to clarify the putative association between CNTN5 CNVs and ASD-risk using large-scale case-control analyses. Method A CNTN5 CNV, shared by four brothers in a multiplex family with ASD, was initially identified. We calculated the prevalence and transmission of CNTN5 CNVs in cases across five ASD cohorts (n=15,784). Second, we compared the prevalence of CNTN5 CNVs in cases to their unaffected siblings (n=4,996). Third, we assessed the enrichment of CNTN5 CNVs in cases to extrafamilial controls across three cohorts (n=24,886) and the UK Biobank (n = 459,862). Finally, we evaluated the clinical impact of CNTN5 CNVs in a broad neurodevelopmental disorder cohort and the DECIPHER database. Results Most (96.7%) CNTN5 CNV deletions (0.193%) and duplications (0.03%) in cases were inherited by a parent that transmitted the variant to their affected and unaffected children at the same rate. We identified a significant enrichment of intronic CNTN5 CNV deletions in cases compared to extrafamilial controls (0.178% versus 0.019%; p-value=1.68E-05; OR:8.51; 95%CI=[2.58-44.21]). There was no difference in CNTN5 CNV enrichment between cases and individuals with NDDs. Conclusions Intronic CNTN5 CNV deletions are rare, inherited, and intermediate effect size ASD-susceptibility variants that may also confer risk for other neuropsychiatric disorders. We offer a framework to characterize candidate variants that may not be detected through small-scale approaches to implicate intermediate effect size variants in the etiology of ASD. En ligne : https://doi.org/10.1016/j.rasd.2022.102055 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490
in Research in Autism Spectrum Disorders > 99 (November) . - 102055[article] Copy-number variants in the contactin-5 gene are a potential risk factor for autism spectrum disorder [Texte imprimé et/ou numérique] / Zoe SCHMILOVICH, Auteur ; Guillaume HUGUET, Auteur ; Qin HE, Auteur ; Amélie MUSA-JOHNSON, Auteur ; Elise DOUARD, Auteur ; Mor Absa LOUM, Auteur ; Calwing LIAO, Auteur ; Jay P. ROSS, Auteur ; Alexandre DIONNE-LAPORTE, Auteur ; Dan SPIEGELMAN, Auteur ; Martineau JEAN-LOUIS, Auteur ; Zohra SACI, Auteur ; Caroline HAYWARD, Auteur ; Tobias BANASCHEWSKI, Auteur ; Arun BOKDE, Auteur ; Sylvane DESRIVIERES, Auteur ; Herve LEMAITRE, Auteur ; Gunter SCHUMANN, Auteur ; Lan XIONG, Auteur ; Patrick A. DION, Auteur ; Sébastien JACQUEMONT, Auteur ; Boris CHAUMETTE, Auteur ; Guy A. ROULEAU, Auteur . - 102055.
Langues : Anglais (eng)
in Research in Autism Spectrum Disorders > 99 (November) . - 102055
Mots-clés : CNTN5 CNV intronic deletions neurodevelopment inherited Index. décimale : PER Périodiques Résumé : Background Contactin-5 (CNTN5) is a candidate risk gene for autism spectrum disorder (ASD). Previous attempts to associate CNTN5 CNVs with ASD-susceptibility were limited by insufficient statistical power. Here, we aim to clarify the putative association between CNTN5 CNVs and ASD-risk using large-scale case-control analyses. Method A CNTN5 CNV, shared by four brothers in a multiplex family with ASD, was initially identified. We calculated the prevalence and transmission of CNTN5 CNVs in cases across five ASD cohorts (n=15,784). Second, we compared the prevalence of CNTN5 CNVs in cases to their unaffected siblings (n=4,996). Third, we assessed the enrichment of CNTN5 CNVs in cases to extrafamilial controls across three cohorts (n=24,886) and the UK Biobank (n = 459,862). Finally, we evaluated the clinical impact of CNTN5 CNVs in a broad neurodevelopmental disorder cohort and the DECIPHER database. Results Most (96.7%) CNTN5 CNV deletions (0.193%) and duplications (0.03%) in cases were inherited by a parent that transmitted the variant to their affected and unaffected children at the same rate. We identified a significant enrichment of intronic CNTN5 CNV deletions in cases compared to extrafamilial controls (0.178% versus 0.019%; p-value=1.68E-05; OR:8.51; 95%CI=[2.58-44.21]). There was no difference in CNTN5 CNV enrichment between cases and individuals with NDDs. Conclusions Intronic CNTN5 CNV deletions are rare, inherited, and intermediate effect size ASD-susceptibility variants that may also confer risk for other neuropsychiatric disorders. We offer a framework to characterize candidate variants that may not be detected through small-scale approaches to implicate intermediate effect size variants in the etiology of ASD. En ligne : https://doi.org/10.1016/j.rasd.2022.102055 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490 Genetics of preparation and response control in ADHD: the role of DRD4 and DAT1 / Björn ALBRECHT in Journal of Child Psychology and Psychiatry, 55-8 (August 2014)
[article]
Titre : Genetics of preparation and response control in ADHD: the role of DRD4 and DAT1 Type de document : Texte imprimé et/ou numérique Auteurs : Björn ALBRECHT, Auteur ; Daniel BRANDEIS, Auteur ; Henrik Uebel VON SANDERSLEBEN, Auteur ; Lilian VALKO, Auteur ; Hartmut HEINRICH, Auteur ; Xiaohui XU, Auteur ; Renate DRECHSLER, Auteur ; Alexander HEISE, Auteur ; Jonna KUNTSI, Auteur ; Ueli C. MÜLLER, Auteur ; Philip ASHERSON, Auteur ; Hans-Christoph STEINHAUSEN, Auteur ; Aribert ROTHENBERGER, Auteur ; Tobias BANASCHEWSKI, Auteur Article en page(s) : p.914-923 Langues : Anglais (eng) Mots-clés : Attention deficit hyperactivity disorder ERP endophenotypes CPT CNV Nogo P3 Index. décimale : PER Périodiques Résumé : Background Difficulties with performance and brain activity related to attentional orienting (Cue-P3), cognitive or response preparation (Cue-CNV) and inhibitory response control (Nogo-P3) during tasks tapping executive functions are familial in ADHD and may represent endophenotypes. The aim of this study was to clarify the impact of dopamine receptor D4 (DRD4) and dopamine transporter (DAT1) gene polymorphisms on these processes in ADHD and control children. Methods Behavioural and electrophysiological parameters from cued continuous performance tests with low and high attentional load were assessed in boys with ADHD combined type (N = 94) and controls without family history of ADHD (N = 31). Both groups were split for the presence of at least one DRD4 7-repeat allele and the DAT1 10-6 haplotype. Results Children with ADHD showed diminished performance and lower Cue-P3, CNV and Nogo-P3 amplitudes. Children with DRD4 7R showed similar performance problems and lower Cue-P3 and CNV, but Nogo-P3 was not reduced. Children with the DAT1 10-6 haplotype had no difficulties with performance or Cue-P3 and CNV, but contrary to expectations increased Nogo-P3. There were no Genotype by ADHD interactions. Conclusions This study detected specific effects of DRD4 7R on performance and brain activity related to attentional orienting and response preparation, while DAT1 10-6 was associated with elevated brain activity related to inhibitory response control, which potentially compensates increased impulsivity. As these genotype effects were additive to the impact of ADHD, the current results indicate that DRD4 and DAT1 polymorphisms are functionally relevant risk factors for ADHD and presumably other disorders sharing these endophenotypes. En ligne : http://dx.doi.org/10.1111/jcpp.12212 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=237
in Journal of Child Psychology and Psychiatry > 55-8 (August 2014) . - p.914-923[article] Genetics of preparation and response control in ADHD: the role of DRD4 and DAT1 [Texte imprimé et/ou numérique] / Björn ALBRECHT, Auteur ; Daniel BRANDEIS, Auteur ; Henrik Uebel VON SANDERSLEBEN, Auteur ; Lilian VALKO, Auteur ; Hartmut HEINRICH, Auteur ; Xiaohui XU, Auteur ; Renate DRECHSLER, Auteur ; Alexander HEISE, Auteur ; Jonna KUNTSI, Auteur ; Ueli C. MÜLLER, Auteur ; Philip ASHERSON, Auteur ; Hans-Christoph STEINHAUSEN, Auteur ; Aribert ROTHENBERGER, Auteur ; Tobias BANASCHEWSKI, Auteur . - p.914-923.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 55-8 (August 2014) . - p.914-923
Mots-clés : Attention deficit hyperactivity disorder ERP endophenotypes CPT CNV Nogo P3 Index. décimale : PER Périodiques Résumé : Background Difficulties with performance and brain activity related to attentional orienting (Cue-P3), cognitive or response preparation (Cue-CNV) and inhibitory response control (Nogo-P3) during tasks tapping executive functions are familial in ADHD and may represent endophenotypes. The aim of this study was to clarify the impact of dopamine receptor D4 (DRD4) and dopamine transporter (DAT1) gene polymorphisms on these processes in ADHD and control children. Methods Behavioural and electrophysiological parameters from cued continuous performance tests with low and high attentional load were assessed in boys with ADHD combined type (N = 94) and controls without family history of ADHD (N = 31). Both groups were split for the presence of at least one DRD4 7-repeat allele and the DAT1 10-6 haplotype. Results Children with ADHD showed diminished performance and lower Cue-P3, CNV and Nogo-P3 amplitudes. Children with DRD4 7R showed similar performance problems and lower Cue-P3 and CNV, but Nogo-P3 was not reduced. Children with the DAT1 10-6 haplotype had no difficulties with performance or Cue-P3 and CNV, but contrary to expectations increased Nogo-P3. There were no Genotype by ADHD interactions. Conclusions This study detected specific effects of DRD4 7R on performance and brain activity related to attentional orienting and response preparation, while DAT1 10-6 was associated with elevated brain activity related to inhibitory response control, which potentially compensates increased impulsivity. As these genotype effects were additive to the impact of ADHD, the current results indicate that DRD4 and DAT1 polymorphisms are functionally relevant risk factors for ADHD and presumably other disorders sharing these endophenotypes. En ligne : http://dx.doi.org/10.1111/jcpp.12212 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=237 A neurophysiological marker of impaired preparation in an 11-year follow-up study of attention-deficit/hyperactivity disorder (ADHD) / Mirko DOEHNERT in Journal of Child Psychology and Psychiatry, 54-3 (March 2013)
[article]
Titre : A neurophysiological marker of impaired preparation in an 11-year follow-up study of attention-deficit/hyperactivity disorder (ADHD) Type de document : Texte imprimé et/ou numérique Auteurs : Mirko DOEHNERT, Auteur ; Daniel BRANDEIS, Auteur ; Gudrun SCHNEIDER, Auteur ; Renate DRECHSLER, Auteur ; Hans-Christoph STEINHAUSEN, Auteur Article en page(s) : p.260-270 Mots-clés : ADHD developmental lag CPT CNV RT-SD Index. décimale : PER Périodiques Résumé : Background: This longitudinal electrophysiological study investigated the course of multiple impaired cognitive brain functions in attention-deficit/hyperactivity disorder (ADHD) from childhood to adulthood by comparing developmental trajectories of individuals with ADHD and typically developing controls. Methods: Subjects with ADHD (N = 11) and normal controls (N = 12) diagnosed in childhood [mean age ADHD/CTRL = 10.9 years [SD 1.72]/10.0 years (SD 1.03)] were followed up after 1.1 and 2.4 years, and as young adults [ADHD/CTRL: 21.9 years (SD 1.46)/21.1 years (SD 1.29)]. At all four times, event-related potential (ERP) maps were recorded during a cued continuous performance test (CPT). We focused on residual deficits as adults, and on developmental trajectories (time and time × group effects) for CPT performance and attentional (Cue P300), preparatory (CNV: contingent negative variation) and inhibitory (NoGo P300) ERP components. Results: All ERP components developed without significant time × group interactions. Only the CNV remained reduced in the ADHD group, although 8/11 individuals no longer met a full ADHD diagnosis as adults. Cue P300 and NoGo P300 group differences became nonsignificant in early adulthood. The CNV parameters correlated with reaction time (RT) and RT-SD. Perceptual sensitivity improved and the groups’ trajectories converged with development, while RT-SD continued to be elevated in adult ADHD subjects. Conclusions: Attentional and preparatory deficits in ADHD continue into adulthood, and the attenuated CNV appears to reflect a particularly stable ADHD marker. Although some deficit reductions may have gone undetected due to small sample size, the findings challenge those developmental lag models postulating that most ADHD-related deficits become negligible with brain maturation. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2012.02572.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=191
in Journal of Child Psychology and Psychiatry > 54-3 (March 2013) . - p.260-270[article] A neurophysiological marker of impaired preparation in an 11-year follow-up study of attention-deficit/hyperactivity disorder (ADHD) [Texte imprimé et/ou numérique] / Mirko DOEHNERT, Auteur ; Daniel BRANDEIS, Auteur ; Gudrun SCHNEIDER, Auteur ; Renate DRECHSLER, Auteur ; Hans-Christoph STEINHAUSEN, Auteur . - p.260-270.
in Journal of Child Psychology and Psychiatry > 54-3 (March 2013) . - p.260-270
Mots-clés : ADHD developmental lag CPT CNV RT-SD Index. décimale : PER Périodiques Résumé : Background: This longitudinal electrophysiological study investigated the course of multiple impaired cognitive brain functions in attention-deficit/hyperactivity disorder (ADHD) from childhood to adulthood by comparing developmental trajectories of individuals with ADHD and typically developing controls. Methods: Subjects with ADHD (N = 11) and normal controls (N = 12) diagnosed in childhood [mean age ADHD/CTRL = 10.9 years [SD 1.72]/10.0 years (SD 1.03)] were followed up after 1.1 and 2.4 years, and as young adults [ADHD/CTRL: 21.9 years (SD 1.46)/21.1 years (SD 1.29)]. At all four times, event-related potential (ERP) maps were recorded during a cued continuous performance test (CPT). We focused on residual deficits as adults, and on developmental trajectories (time and time × group effects) for CPT performance and attentional (Cue P300), preparatory (CNV: contingent negative variation) and inhibitory (NoGo P300) ERP components. Results: All ERP components developed without significant time × group interactions. Only the CNV remained reduced in the ADHD group, although 8/11 individuals no longer met a full ADHD diagnosis as adults. Cue P300 and NoGo P300 group differences became nonsignificant in early adulthood. The CNV parameters correlated with reaction time (RT) and RT-SD. Perceptual sensitivity improved and the groups’ trajectories converged with development, while RT-SD continued to be elevated in adult ADHD subjects. Conclusions: Attentional and preparatory deficits in ADHD continue into adulthood, and the attenuated CNV appears to reflect a particularly stable ADHD marker. Although some deficit reductions may have gone undetected due to small sample size, the findings challenge those developmental lag models postulating that most ADHD-related deficits become negligible with brain maturation. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2012.02572.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=191 A Deletion Involving CD38 and BST1 Results in a Fusion Transcript in a Patient With Autism and Asthma / Fabiola CERONI in Autism Research, 7-2 (April 2014)
[article]
Titre : A Deletion Involving CD38 and BST1 Results in a Fusion Transcript in a Patient With Autism and Asthma Type de document : Texte imprimé et/ou numérique Auteurs : Fabiola CERONI, Auteur ; Angela SAGAR, Auteur ; Nuala H. SIMPSON, Auteur ; Alex J. T. GAWTHROPE, Auteur ; Dianne F. NEWBURY, Auteur ; Dalila PINTO, Auteur ; Sunday M. FRANCIS, Auteur ; Dorothy C. TESSMAN, Auteur ; Edwin H. Jr COOK, Auteur ; Anthony P. MONACO, Auteur ; Elena MAESTRINI, Auteur ; Alistair T. PAGNAMENTA, Auteur ; Suma JACOB, Auteur Article en page(s) : p.254-263 Mots-clés : autism CD38 oxytocin CNV fusion transcript Index. décimale : PER Périodiques Résumé : CD38 encodes a ligand in the oxytocin signaling pathway. Some single nucleotide polymorphisms in this gene have been associated with low serum oxytocin levels in autism spectrum disorder (ASD) patients. Oxytocin disruption has been hypothesized to account for features of ASD, including impaired communication and social behavior, based on animal studies. Recent human studies have shown administration of oxytocin improving emotion recognition, promoting social behavior, and improving auditory processing of social stimuli in ASD patients. In addition to its role in oxytocin signaling, CD38 is involved in the regulation of calcium concentration in airway smooth muscle with impairment of CD38 being implicated in airway diseases like asthma. While a number of studies have implicated rare chromosomal deletions and duplications in helping determine genetic risk for autism, there are to our knowledge no reports describing rearrangements involving CD38 or deletions in patients with ASD. Here, we present two sisters diagnosed with autism and with features of regression—previously acquired speech lost in the second year of life. The younger sister, who also had asthma, inherited a maternal deletion of 4p15.32 that results in a BST1-CD38 fusion transcript. Their mother's deletion was mosaic and she was not affected. Although further work is required to assess functional consequences of the fusion transcript, we hypothesize that the proband's deletion may have served as a risk factor for autism that, when combined with other susceptibility variants, resulted in a more severe presentation than her sister. En ligne : http://dx.doi.org/10.1002/aur.1365 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=230
in Autism Research > 7-2 (April 2014) . - p.254-263[article] A Deletion Involving CD38 and BST1 Results in a Fusion Transcript in a Patient With Autism and Asthma [Texte imprimé et/ou numérique] / Fabiola CERONI, Auteur ; Angela SAGAR, Auteur ; Nuala H. SIMPSON, Auteur ; Alex J. T. GAWTHROPE, Auteur ; Dianne F. NEWBURY, Auteur ; Dalila PINTO, Auteur ; Sunday M. FRANCIS, Auteur ; Dorothy C. TESSMAN, Auteur ; Edwin H. Jr COOK, Auteur ; Anthony P. MONACO, Auteur ; Elena MAESTRINI, Auteur ; Alistair T. PAGNAMENTA, Auteur ; Suma JACOB, Auteur . - p.254-263.
in Autism Research > 7-2 (April 2014) . - p.254-263
Mots-clés : autism CD38 oxytocin CNV fusion transcript Index. décimale : PER Périodiques Résumé : CD38 encodes a ligand in the oxytocin signaling pathway. Some single nucleotide polymorphisms in this gene have been associated with low serum oxytocin levels in autism spectrum disorder (ASD) patients. Oxytocin disruption has been hypothesized to account for features of ASD, including impaired communication and social behavior, based on animal studies. Recent human studies have shown administration of oxytocin improving emotion recognition, promoting social behavior, and improving auditory processing of social stimuli in ASD patients. In addition to its role in oxytocin signaling, CD38 is involved in the regulation of calcium concentration in airway smooth muscle with impairment of CD38 being implicated in airway diseases like asthma. While a number of studies have implicated rare chromosomal deletions and duplications in helping determine genetic risk for autism, there are to our knowledge no reports describing rearrangements involving CD38 or deletions in patients with ASD. Here, we present two sisters diagnosed with autism and with features of regression—previously acquired speech lost in the second year of life. The younger sister, who also had asthma, inherited a maternal deletion of 4p15.32 that results in a BST1-CD38 fusion transcript. Their mother's deletion was mosaic and she was not affected. Although further work is required to assess functional consequences of the fusion transcript, we hypothesize that the proband's deletion may have served as a risk factor for autism that, when combined with other susceptibility variants, resulted in a more severe presentation than her sister. En ligne : http://dx.doi.org/10.1002/aur.1365 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=230
in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA
Titre : Genetic Causes of Autism Spectrum Disorders Type de document : Texte imprimé et/ou numérique Auteurs : Guillaume HUGUET, Auteur ; Thomas BOURGERON, Auteur Année de publication : 2016 Importance : p.13-24 Langues : Anglais (eng) Mots-clés : Autism spectrum disorders CNV Heritability SNV Synapse Twin studies Index. décimale : SCI-D SCI-D - Neurosciences Résumé : In the past 30 years, twin studies have indicated a strong genetic contribution to autism spectrum disorders (ASD). The heritability of ASD is estimated to be 50%. Whereas most of the inherited part of ASD is captured by common variants, our knowledge about the genetics of ASD comes almost exclusively from identification of highly penetrant de novo mutations through candidate gene or whole exome/genome sequencing studies. Approximately 10% of patients with ASD, especially those with intellectual disability, are carriers of de novo copy number or single nucleotide variants affecting clinically relevant genes for ASD. Because of the function of these genes, it was hypothesized that abnormal synaptic plasticity and failure of neuronal/synaptic homeostasis could increase the risk of ASD. It is hoped that this knowledge will lead to better diagnosis, care, and integration of individuals with ASD. En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00002-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301 Genetic Causes of Autism Spectrum Disorders [Texte imprimé et/ou numérique] / Guillaume HUGUET, Auteur ; Thomas BOURGERON, Auteur . - 2016 . - p.13-24.
in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA
Langues : Anglais (eng)
Mots-clés : Autism spectrum disorders CNV Heritability SNV Synapse Twin studies Index. décimale : SCI-D SCI-D - Neurosciences Résumé : In the past 30 years, twin studies have indicated a strong genetic contribution to autism spectrum disorders (ASD). The heritability of ASD is estimated to be 50%. Whereas most of the inherited part of ASD is captured by common variants, our knowledge about the genetics of ASD comes almost exclusively from identification of highly penetrant de novo mutations through candidate gene or whole exome/genome sequencing studies. Approximately 10% of patients with ASD, especially those with intellectual disability, are carriers of de novo copy number or single nucleotide variants affecting clinically relevant genes for ASD. Because of the function of these genes, it was hypothesized that abnormal synaptic plasticity and failure of neuronal/synaptic homeostasis could increase the risk of ASD. It is hoped that this knowledge will lead to better diagnosis, care, and integration of individuals with ASD. En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00002-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301 Exemplaires
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