32 recherche sur le mot-clé 'serotonin'

Serotonin Hypothesis of Autism: Implications for Selective Serotonin Reuptake Inhibitor Use during Pregnancy / Rebecca A. HARRINGTON in Autism Research, 6-3 (June 2013)  

Public ISBD [article]  inAutism Research > 6-3 (June 2013) . - p.149-168 Titre : Serotonin Hypothesis of Autism: Implications for Selective Serotonin Reuptake Inhibitor Use during Pregnancy Type de document : texte imprimé Auteurs : Rebecca A. HARRINGTON, Auteur ; Li-Ching LEE, Auteur ; Rosa M. CRUM, Auteur ; Andrew W. ZIMMERMAN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur Année de publication : 2013 Article en page(s) : p.149-168 Langues : Anglais (eng) Mots-clés : autism spectrum disorders  serotonin  selective serotonin reuptake inhibitors  pregnancy Index. décimale : PER Périodiques Résumé : Serotonin, a neurotransmitter found throughout the brain and body, has long been of interest in autism. Repeated findings of elevated platelet serotonin levels in approximately one third of children with autism has led some to believe that dysfunctional serotonin signaling may be a causal mechanism for the disorder. Because serotonin is critical to fetal brain development, concerns have arisen regarding prenatal exposure to substances that manipulate serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs). This review examines evidence regarding the serotonin system and autism spectrum disorders (ASD), as well as what the literature has reported thus far on developmental effects of prenatal exposure to SSRIs. Possible mechanisms by which SSRIs could affect the fetus during pregnancy and clinical implications are also discussed. Though the majority of studies conducted in infants and children suggest prenatal exposure to SSRIs does not affect neurodevelopment, interpretation must be tempered given small sample sizes. The only published study that focused on prenatal SSRI exposure and ASD found an increased risk with exposure to SSRIs, especially during the first trimester. Obstacles that will be faced in future research are isolating medication effects from maternal depression and, given the infrequent occurrence of exposure and outcome, obtaining an adequate sample size. Whether serotonin is an etiologic factor in ASD, and what it points to as a marker for subgrouping, remains unclear. Understanding how the development of ASD might be affected by prenatal factors that influence serotonin levels, such as SSRIs, could identify modifiable targets for prevention. En ligne : http://dx.doi.org/10.1002/aur.1288 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202 [article] Serotonin Hypothesis of Autism: Implications for Selective Serotonin Reuptake Inhibitor Use during Pregnancy [texte imprimé] / Rebecca A. HARRINGTON, Auteur ; Li-Ching LEE, Auteur ; Rosa M. CRUM, Auteur ; Andrew W. ZIMMERMAN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur . - 2013 . - p.149-168. Langues : Anglais (eng) in Autism Research > 6-3 (June 2013) . - p.149-168 Mots-clés : autism spectrum disorders  serotonin  selective serotonin reuptake inhibitors  pregnancy Index. décimale : PER Périodiques Résumé : Serotonin, a neurotransmitter found throughout the brain and body, has long been of interest in autism. Repeated findings of elevated platelet serotonin levels in approximately one third of children with autism has led some to believe that dysfunctional serotonin signaling may be a causal mechanism for the disorder. Because serotonin is critical to fetal brain development, concerns have arisen regarding prenatal exposure to substances that manipulate serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs). This review examines evidence regarding the serotonin system and autism spectrum disorders (ASD), as well as what the literature has reported thus far on developmental effects of prenatal exposure to SSRIs. Possible mechanisms by which SSRIs could affect the fetus during pregnancy and clinical implications are also discussed. Though the majority of studies conducted in infants and children suggest prenatal exposure to SSRIs does not affect neurodevelopment, interpretation must be tempered given small sample sizes. The only published study that focused on prenatal SSRI exposure and ASD found an increased risk with exposure to SSRIs, especially during the first trimester. Obstacles that will be faced in future research are isolating medication effects from maternal depression and, given the infrequent occurrence of exposure and outcome, obtaining an adequate sample size. Whether serotonin is an etiologic factor in ASD, and what it points to as a marker for subgrouping, remains unclear. Understanding how the development of ASD might be affected by prenatal factors that influence serotonin levels, such as SSRIs, could identify modifiable targets for prevention. En ligne : http://dx.doi.org/10.1002/aur.1288 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202

Serotonin dysfunction in ADHD / Eleanor F. JACKSON in Journal of Neurodevelopmental Disorders, 17 (2025)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 17 (2025) Titre : Serotonin dysfunction in ADHD Type de document : texte imprimé Auteurs : Eleanor F. JACKSON, Auteur ; Timothy B. RILEY, Auteur ; Paul G. OVERTON, Auteur Langues : Anglais (eng) Mots-clés : Attention Deficit Disorder with Hyperactivity/metabolism/drug  therapy/physiopathology  Humans  Serotonin/metabolism  Tryptophan/metabolism  Animals  Synaptic Transmission/physiology  5-hydroxytryptophan.  Attention deficit hyperactivity disorder  Kynurenine  Serotonin  Tryptophan  for publication: Not applicable. Competing interests: The authors declare no  competing interests. Index. décimale : PER Périodiques Résumé : It is well accepted that attention deficit hyperactivity disorder (ADHD) is in part driven by dysfunction in the monoaminergic neurotransmitter system, but both the extent of dysfunction and possible therapeutic avenues presented by serotonergic neurotransmission is frequently overlooked. As such, we present key evidence for dysfunction in serotonergic transmission, as seen from biochemical, genetic and pharmacological perspectives. An overall deficit in serotonin availability is a common theme throughout the literature, thus this review aims to explore possible dysfunctions in the serotonin synthesis pathway which result in this reduced bioavailability, and investigate whether such dysfunctions could be loci of change in ADHD. We have identified several steps in transmission, namely the conversion of tryptophan to 5-hydroxytryptophan and its use of cofactor tetrahydrobiopterin, which could present promising avenues for development of novel clinical interventions for ADHD. En ligne : https://dx.doi.org/10.1186/s11689-025-09610-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576 [article] Serotonin dysfunction in ADHD [texte imprimé] / Eleanor F. JACKSON, Auteur ; Timothy B. RILEY, Auteur ; Paul G. OVERTON, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 17 (2025) Mots-clés : Attention Deficit Disorder with Hyperactivity/metabolism/drug  therapy/physiopathology  Humans  Serotonin/metabolism  Tryptophan/metabolism  Animals  Synaptic Transmission/physiology  5-hydroxytryptophan.  Attention deficit hyperactivity disorder  Kynurenine  Serotonin  Tryptophan  for publication: Not applicable. Competing interests: The authors declare no  competing interests. Index. décimale : PER Périodiques Résumé : It is well accepted that attention deficit hyperactivity disorder (ADHD) is in part driven by dysfunction in the monoaminergic neurotransmitter system, but both the extent of dysfunction and possible therapeutic avenues presented by serotonergic neurotransmission is frequently overlooked. As such, we present key evidence for dysfunction in serotonergic transmission, as seen from biochemical, genetic and pharmacological perspectives. An overall deficit in serotonin availability is a common theme throughout the literature, thus this review aims to explore possible dysfunctions in the serotonin synthesis pathway which result in this reduced bioavailability, and investigate whether such dysfunctions could be loci of change in ADHD. We have identified several steps in transmission, namely the conversion of tryptophan to 5-hydroxytryptophan and its use of cofactor tetrahydrobiopterin, which could present promising avenues for development of novel clinical interventions for ADHD. En ligne : https://dx.doi.org/10.1186/s11689-025-09610-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576

Analysis of neuroanatomical differences in mice with genetically modified serotonin transporters assessed by structural magnetic resonance imaging / Jacob ELLEGOOD in Molecular Autism, 9 (2018)  

Public ISBD [article]  inMolecular Autism > 9 (2018) . - 24p. Titre : Analysis of neuroanatomical differences in mice with genetically modified serotonin transporters assessed by structural magnetic resonance imaging Type de document : texte imprimé Auteurs : Jacob ELLEGOOD, Auteur ; Yohan YEE, Auteur ; Travis KERR, Auteur ; Christopher L. MULLER, Auteur ; Randy D. BLAKELY, Auteur ; R. Mark HENKELMAN, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur ; Jason P. LERCH, Auteur Article en page(s) : 24p. Langues : Anglais (eng) Mots-clés : Animals  Brain/diagnostic imaging/metabolism  Female  Magnetic Resonance Imaging  Male  Mice  Mice, Inbred C57BL  Mutation  Neurons/metabolism  Serotonin/metabolism  Serotonin Plasma Membrane Transport Proteins/genetics/metabolism  5-ht  5htt  Brain  Dorsal raphe  Magnetic resonance imaging  Neurodevelopment  Serotonin  Slc6a4 Index. décimale : PER Périodiques Résumé : Background: The serotonin (5-HT) system has long been implicated in autism spectrum disorder (ASD) as indicated by elevated whole blood and platelet 5-HT, altered platelet and brain receptor and transporter binding, and genetic linkage and association findings. Based upon work in genetically modified mice, 5-HT is known to influence several aspects of brain development, but systematic neuroimaging studies have not previously been reported. In particular, the 5-HT transporter (serotonin transporter, SERT; 5-HTT) gene, Slc6a4, has been extensively studied. Methods: Using a 7-T MRI and deformation-based morphometry, we assessed neuroanatomical differences in an Slc6a4 knockout mouse on a C57BL/6 genetic background, along with an Slc6a4 Ala56 knockin mouse on two different genetic backgrounds (129S and C57BL/6). Results: Individually (same sex, same background, same genotype), the only differences found were in the female Slc6a4 knockout mouse; all the others had no significant differences. However, an analysis of variance across the whole study sample revealed a significant effect of Slc6a4 on the amygdala, thalamus, dorsal raphe nucleus, and lateral and frontal cortices. Conclusions: This work shows that an increase or decrease in SERT function has a significant effect on the neuroanatomy in 5-HT relevant regions, particularly the raphe nuclei. Notably, the Slc6a4 Ala56 knockin alone appears to have an insignificant, but suggestive, effect compared to the KO, which is consistent with Slc6a4 function. Despite the small number of 5-HT neurons and their localization to the brainstem, it is clear that 5-HT plays an important role in neuroanatomical organization. En ligne : https://dx.doi.org/10.1186/s13229-018-0210-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 [article] Analysis of neuroanatomical differences in mice with genetically modified serotonin transporters assessed by structural magnetic resonance imaging [texte imprimé] / Jacob ELLEGOOD, Auteur ; Yohan YEE, Auteur ; Travis KERR, Auteur ; Christopher L. MULLER, Auteur ; Randy D. BLAKELY, Auteur ; R. Mark HENKELMAN, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur ; Jason P. LERCH, Auteur . - 24p. Langues : Anglais (eng) in Molecular Autism > 9 (2018) . - 24p. Mots-clés : Animals  Brain/diagnostic imaging/metabolism  Female  Magnetic Resonance Imaging  Male  Mice  Mice, Inbred C57BL  Mutation  Neurons/metabolism  Serotonin/metabolism  Serotonin Plasma Membrane Transport Proteins/genetics/metabolism  5-ht  5htt  Brain  Dorsal raphe  Magnetic resonance imaging  Neurodevelopment  Serotonin  Slc6a4 Index. décimale : PER Périodiques Résumé : Background: The serotonin (5-HT) system has long been implicated in autism spectrum disorder (ASD) as indicated by elevated whole blood and platelet 5-HT, altered platelet and brain receptor and transporter binding, and genetic linkage and association findings. Based upon work in genetically modified mice, 5-HT is known to influence several aspects of brain development, but systematic neuroimaging studies have not previously been reported. In particular, the 5-HT transporter (serotonin transporter, SERT; 5-HTT) gene, Slc6a4, has been extensively studied. Methods: Using a 7-T MRI and deformation-based morphometry, we assessed neuroanatomical differences in an Slc6a4 knockout mouse on a C57BL/6 genetic background, along with an Slc6a4 Ala56 knockin mouse on two different genetic backgrounds (129S and C57BL/6). Results: Individually (same sex, same background, same genotype), the only differences found were in the female Slc6a4 knockout mouse; all the others had no significant differences. However, an analysis of variance across the whole study sample revealed a significant effect of Slc6a4 on the amygdala, thalamus, dorsal raphe nucleus, and lateral and frontal cortices. Conclusions: This work shows that an increase or decrease in SERT function has a significant effect on the neuroanatomy in 5-HT relevant regions, particularly the raphe nuclei. Notably, the Slc6a4 Ala56 knockin alone appears to have an insignificant, but suggestive, effect compared to the KO, which is consistent with Slc6a4 function. Despite the small number of 5-HT neurons and their localization to the brainstem, it is clear that 5-HT plays an important role in neuroanatomical organization. En ligne : https://dx.doi.org/10.1186/s13229-018-0210-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371

Serotonin and early cognitive development: variation in the tryptophan hydroxylase 2 gene is associated with visual attention in 7-month-old infants / Jukka M. LEPPANEN in Journal of Child Psychology and Psychiatry, 52-11 (November 2011)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 52-11 (November 2011) . - p.1144-1152 Titre : Serotonin and early cognitive development: variation in the tryptophan hydroxylase 2 gene is associated with visual attention in 7-month-old infants Type de document : texte imprimé Auteurs : Jukka M. LEPPANEN, Auteur ; Mikko J. PELTOLA, Auteur ; Kaija PUURA, Auteur ; Mirjami MANTYMAA, Auteur ; Nina MONONEN, Auteur ; Terho LEHTIMAKI, Auteur Année de publication : 2011 Article en page(s) : p.1144-1152 Langues : Anglais (eng) Mots-clés : Attention  cognition  development  emotion  infancy  serotonin Index. décimale : PER Périodiques Résumé : Background:  Allelic variation in the promoter region of a gene that encodes tryptophan hydroxylase isoform 2 (TPH2), a rate-limiting enzyme of serotonin synthesis in the central nervous system, has been associated with variations in cognitive function and vulnerability to affective spectrum disorders. Little is known about the effects of this gene variant on cognition during development and about possible intermediate developmental steps that lead to the adult phenotype. Here, we examined the hypothesis that the TPH2 -703 may act during early stages of development and bias the acquisition of elementary cognitive processes involved in attention and emotion regulation. Methods:  Seven-month-old infants (n = 66) were genotyped for the TPH2 -703 G/T polymorphism (rs4570625) and tested for the efficiency of attention shifts from a stimulus at fixation to a new stimulus in the visual periphery. Results:  Compared to TPH2 G/G homozygotes, infants with the T-carrier genotype exhibited a significantly higher number of missing attention shifts. This genotype effect tended to be particularly pronounced when infants had to disengage from an affectively salient stimulus before shifting attention to the peripheral stimulus. The results also showed that TPH2 genotype was indirectly associated, via its effect on attention disengagement, with temperamental emotion regulation (soothability). Conclusions:  Together, these results implicate serotonin system genes in early cognitive development and suggest variations in the early-emerging cognitive capacities as a potential developmental precursor of individual differences in emotion regulation and vulnerability to affective disorders. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02391.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=145 [article] Serotonin and early cognitive development: variation in the tryptophan hydroxylase 2 gene is associated with visual attention in 7-month-old infants [texte imprimé] / Jukka M. LEPPANEN, Auteur ; Mikko J. PELTOLA, Auteur ; Kaija PUURA, Auteur ; Mirjami MANTYMAA, Auteur ; Nina MONONEN, Auteur ; Terho LEHTIMAKI, Auteur . - 2011 . - p.1144-1152. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 52-11 (November 2011) . - p.1144-1152 Mots-clés : Attention  cognition  development  emotion  infancy  serotonin Index. décimale : PER Périodiques Résumé : Background:  Allelic variation in the promoter region of a gene that encodes tryptophan hydroxylase isoform 2 (TPH2), a rate-limiting enzyme of serotonin synthesis in the central nervous system, has been associated with variations in cognitive function and vulnerability to affective spectrum disorders. Little is known about the effects of this gene variant on cognition during development and about possible intermediate developmental steps that lead to the adult phenotype. Here, we examined the hypothesis that the TPH2 -703 may act during early stages of development and bias the acquisition of elementary cognitive processes involved in attention and emotion regulation. Methods:  Seven-month-old infants (n = 66) were genotyped for the TPH2 -703 G/T polymorphism (rs4570625) and tested for the efficiency of attention shifts from a stimulus at fixation to a new stimulus in the visual periphery. Results:  Compared to TPH2 G/G homozygotes, infants with the T-carrier genotype exhibited a significantly higher number of missing attention shifts. This genotype effect tended to be particularly pronounced when infants had to disengage from an affectively salient stimulus before shifting attention to the peripheral stimulus. The results also showed that TPH2 genotype was indirectly associated, via its effect on attention disengagement, with temperamental emotion regulation (soothability). Conclusions:  Together, these results implicate serotonin system genes in early cognitive development and suggest variations in the early-emerging cognitive capacities as a potential developmental precursor of individual differences in emotion regulation and vulnerability to affective disorders. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02391.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=145

Serotonin transporter-linked polymorphic region (5-HTTLPR) genotype and stressful life events interact to predict preschool-onset depression: a replication and developmental extension / Ryan BOGDAN in Journal of Child Psychology and Psychiatry, 55-5 (May 2014)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 55-5 (May 2014) . - p.448-457 Titre : Serotonin transporter-linked polymorphic region (5-HTTLPR) genotype and stressful life events interact to predict preschool-onset depression: a replication and developmental extension Type de document : texte imprimé Auteurs : Ryan BOGDAN, Auteur ; Arpana AGRAWAL, Auteur ; Michael S. GAFFREY, Auteur ; Rebecca TILLMAN, Auteur ; Joan L. LUBY, Auteur Article en page(s) : p.448-457 Mots-clés : Depression  stress  5-HTTLPR  serotonin  gene*  interaction  plasticity  childhood  development  gene × environment Index. décimale : PER Périodiques Résumé : Background Scientific enthusiasm about gene × environment interactions, spurred by the 5-HTTLPR (serotonin transporter-linked polymorphic region) × SLEs (stressful life events) interaction predicting depression, have recently been tempered by sober realizations of small effects and meta-analyses reaching opposing conclusions. These mixed findings highlight the need for further research. Converging evidence suggests that the effects of 5-HTTLPR genotype may be neurodevelopmental in origin, but we are not aware of empirical studies that have investigated whether the 5-HTTLPR genotype × SLE interaction predicts preschool-onset depression (PO-MDD), the earliest validated form of depression. Methods Children (n = 234) aged 3–5 were recruited for a longitudinal study designed to examine PO-MDD. In a comprehensive baseline assessment, the child's primary caregivers completed questionnaires and were interviewed about their child's behaviors, psychiatric symptoms, and exposure to SLEs. Results A 5-HTTLPR × SLEs interaction emerged, such that children homozygous for the short allele were more susceptible to depression in the context of elevated SLE than long allele carriers. In contrast, at low SLE exposure, short allele homozygotes had fewer depressive symptoms. The data were best fit by a plasticity model with a substantial reduction in fit by diathesis-stress models. Conclusions Extending studies in adult and adolescent populations, these data suggest that 5-HTTLPR genotype may provide plasticity to environmental influence, for better or worse. Specifically, children homozygous for the short allele were more susceptible to the depressogenic effects of SLEs but benefitted, in the form of reduced depressive symptoms, in the context of relatively benign environmental conditions (i.e. relatively low SLE exposure). These data highlight the importance of examining gene × environment interactions across development, environment, and outcome but should be interpreted cautiously given the small sample size. En ligne : http://dx.doi.org/10.1111/jcpp.12142 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=231 [article] Serotonin transporter-linked polymorphic region (5-HTTLPR) genotype and stressful life events interact to predict preschool-onset depression: a replication and developmental extension [texte imprimé] / Ryan BOGDAN, Auteur ; Arpana AGRAWAL, Auteur ; Michael S. GAFFREY, Auteur ; Rebecca TILLMAN, Auteur ; Joan L. LUBY, Auteur . - p.448-457. in Journal of Child Psychology and Psychiatry > 55-5 (May 2014) . - p.448-457 Mots-clés : Depression  stress  5-HTTLPR  serotonin  gene*  interaction  plasticity  childhood  development  gene × environment Index. décimale : PER Périodiques Résumé : Background Scientific enthusiasm about gene × environment interactions, spurred by the 5-HTTLPR (serotonin transporter-linked polymorphic region) × SLEs (stressful life events) interaction predicting depression, have recently been tempered by sober realizations of small effects and meta-analyses reaching opposing conclusions. These mixed findings highlight the need for further research. Converging evidence suggests that the effects of 5-HTTLPR genotype may be neurodevelopmental in origin, but we are not aware of empirical studies that have investigated whether the 5-HTTLPR genotype × SLE interaction predicts preschool-onset depression (PO-MDD), the earliest validated form of depression. Methods Children (n = 234) aged 3–5 were recruited for a longitudinal study designed to examine PO-MDD. In a comprehensive baseline assessment, the child's primary caregivers completed questionnaires and were interviewed about their child's behaviors, psychiatric symptoms, and exposure to SLEs. Results A 5-HTTLPR × SLEs interaction emerged, such that children homozygous for the short allele were more susceptible to depression in the context of elevated SLE than long allele carriers. In contrast, at low SLE exposure, short allele homozygotes had fewer depressive symptoms. The data were best fit by a plasticity model with a substantial reduction in fit by diathesis-stress models. Conclusions Extending studies in adult and adolescent populations, these data suggest that 5-HTTLPR genotype may provide plasticity to environmental influence, for better or worse. Specifically, children homozygous for the short allele were more susceptible to the depressogenic effects of SLEs but benefitted, in the form of reduced depressive symptoms, in the context of relatively benign environmental conditions (i.e. relatively low SLE exposure). These data highlight the importance of examining gene × environment interactions across development, environment, and outcome but should be interpreted cautiously given the small sample size. En ligne : http://dx.doi.org/10.1111/jcpp.12142 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=231

Acute administration of NLX-101, a Serotonin 1A receptor agonist, improves auditory temporal processing during development in a mouse model of Fragile X Syndrome / Xin TAO in Journal of Neurodevelopmental Disorders, 17 (2025)  

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Brief Report: Platelet-Poor Plasma Serotonin in Autism / George M. ANDERSON in Journal of Autism and Developmental Disorders, 42-7 (July 2012)  

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Brief Report: Whole Blood Serotonin Levels and Gastrointestinal Symptoms in Autism Spectrum Disorder / Sarah MARLER in Journal of Autism and Developmental Disorders, 46-3 (March 2016)  

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Family-Based Clinical Associations and Functional Characterization of the Serotonin 2A Receptor Gene (HTR2A) in Autism Spectrum Disorder / Ryan M. SMITH in Autism Research, 7-4 (August 2014)  

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Intestinal Predictors of Whole Blood Serotonin Levels in Children With or Without Autism / Miranda ZUNIGA-KENNEDY in Journal of Autism and Developmental Disorders, 52-9 (September 2022)  

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