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Associations of endocrine stress-related gene polymorphisms with risk of autism spectrum disorders: Evidence from an integrated meta-analysis / Ping-yuan YANG in Autism Research, 10-11 (November 2017)
[article]
Titre : Associations of endocrine stress-related gene polymorphisms with risk of autism spectrum disorders: Evidence from an integrated meta-analysis Type de document : Texte imprimé et/ou numérique Auteurs : Ping-yuan YANG, Auteur ; Ya-jing MENGA, Auteur ; Tao LI, Auteur ; Yi HUANG, Auteur Article en page(s) : p.1722-1736 Langues : Anglais (eng) Mots-clés : autism spectrum disorders (ASD) catechol-O-methyl transferase (COMT) serotonin transporter stress response Index. décimale : PER Périodiques Résumé : Autism spectrum disorders (ASD) are related to serotonin transporter (5-HTT) and catechol-O-methyl transferase (COMT) as two most monoaminergic polymorphic variations. However, multiple studies assessing rs4680 and 5-HTTLPR variants in ASD have reported inconsistent results. Therefore, we conducted an integrated meta-analysis to combine case-control and transmission/disequilibrium test (TDT) studies to determine whether COMT and 5-HTT are associated with ASD. We searched multiple electronic databases (PubMed, EmBase and Web of Science) to identify studies assessing the rs4680 and 5-HTTLPR variants in ASD from Jan 1997 to Dec 2016. Then allelic data from case–control and TDT studies were analyzed by the Catmap package in the R software. A total of 5 studies were eligible for the meta-analysis of rs4680, including 3 case–control, 1 TDT and 1 TDT & case–control studies. Meanwhile, 22 studies of 5-HTTLPR were available, including 16 TDT, 4 case–control and 2 TDT & case–control studies. The current meta-analysis included 814 ASD cases, 741 controls and 311 families related to rs4680; 749 ASD cases, 1,118 controls and 1,861 families relevant to 5-HTTLPR were also evaluated. For rs4680, the pooled OR was 1.18 (95% CI?=?0.87–1.59, P?=?0.29, Pheterogeneity?0.00001). There was no significant association of rs4680 with risk of ASD between the two subgroups. For 5-HTTLPR, the pooled OR was 1.05 (95% CI?=?0.92–1.20, P?=?0.4652, Pheterogeneity?0.00001). Meanwhile, we found no significant risk in individual case–control or TDT studies. The above findings indicated that neither COMT rs4680 nor 5-HTT 5-HTTLPR polymorphism significantly affects ASD risk. Autism Res 2017, 10: 1722–1736. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary Our results showed no evidence of significant association of either COMT rs4680 or 5-HTT 5-HTTLPR variants with ASD, showing that these two genes may not be major susceptible genetic factors in ASD occurrence, and may have a reciprocal action with each other in combination with environmental factors. These findings further provide evidence that a single gene variant may not dictate autism occurrence, but possibly contributes to a specific phenotype or subtype of ASD. En ligne : http://dx.doi.org/10.1002/aur.1822 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=322
in Autism Research > 10-11 (November 2017) . - p.1722-1736[article] Associations of endocrine stress-related gene polymorphisms with risk of autism spectrum disorders: Evidence from an integrated meta-analysis [Texte imprimé et/ou numérique] / Ping-yuan YANG, Auteur ; Ya-jing MENGA, Auteur ; Tao LI, Auteur ; Yi HUANG, Auteur . - p.1722-1736.
Langues : Anglais (eng)
in Autism Research > 10-11 (November 2017) . - p.1722-1736
Mots-clés : autism spectrum disorders (ASD) catechol-O-methyl transferase (COMT) serotonin transporter stress response Index. décimale : PER Périodiques Résumé : Autism spectrum disorders (ASD) are related to serotonin transporter (5-HTT) and catechol-O-methyl transferase (COMT) as two most monoaminergic polymorphic variations. However, multiple studies assessing rs4680 and 5-HTTLPR variants in ASD have reported inconsistent results. Therefore, we conducted an integrated meta-analysis to combine case-control and transmission/disequilibrium test (TDT) studies to determine whether COMT and 5-HTT are associated with ASD. We searched multiple electronic databases (PubMed, EmBase and Web of Science) to identify studies assessing the rs4680 and 5-HTTLPR variants in ASD from Jan 1997 to Dec 2016. Then allelic data from case–control and TDT studies were analyzed by the Catmap package in the R software. A total of 5 studies were eligible for the meta-analysis of rs4680, including 3 case–control, 1 TDT and 1 TDT & case–control studies. Meanwhile, 22 studies of 5-HTTLPR were available, including 16 TDT, 4 case–control and 2 TDT & case–control studies. The current meta-analysis included 814 ASD cases, 741 controls and 311 families related to rs4680; 749 ASD cases, 1,118 controls and 1,861 families relevant to 5-HTTLPR were also evaluated. For rs4680, the pooled OR was 1.18 (95% CI?=?0.87–1.59, P?=?0.29, Pheterogeneity?0.00001). There was no significant association of rs4680 with risk of ASD between the two subgroups. For 5-HTTLPR, the pooled OR was 1.05 (95% CI?=?0.92–1.20, P?=?0.4652, Pheterogeneity?0.00001). Meanwhile, we found no significant risk in individual case–control or TDT studies. The above findings indicated that neither COMT rs4680 nor 5-HTT 5-HTTLPR polymorphism significantly affects ASD risk. Autism Res 2017, 10: 1722–1736. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary Our results showed no evidence of significant association of either COMT rs4680 or 5-HTT 5-HTTLPR variants with ASD, showing that these two genes may not be major susceptible genetic factors in ASD occurrence, and may have a reciprocal action with each other in combination with environmental factors. These findings further provide evidence that a single gene variant may not dictate autism occurrence, but possibly contributes to a specific phenotype or subtype of ASD. En ligne : http://dx.doi.org/10.1002/aur.1822 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=322 Brain hyperserotonemia causes autism-relevant social deficits in mice / M. TANAKA in Molecular Autism, 9 (2018)
[article]
Titre : Brain hyperserotonemia causes autism-relevant social deficits in mice Type de document : Texte imprimé et/ou numérique Auteurs : M. TANAKA, Auteur ; A. SATO, Auteur ; S. KASAI, Auteur ; Y. HAGINO, Auteur ; H. KOTAJIMA-MURAKAMI, Auteur ; H. KASHII, Auteur ; Y. TAKAMATSU, Auteur ; Y. NISHITO, Auteur ; M. INAGAKI, Auteur ; M. MIZUGUCHI, Auteur ; F. S. HALL, Auteur ; G. R. UHL, Auteur ; D. MURPHY, Auteur ; I. SORA, Auteur ; K. IKEDA, Auteur Article en page(s) : 60p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Heterozygous mice Serotonin transporter Tryptophan depletion Index. décimale : PER Périodiques Résumé : Background: Hyperserotonemia in the brain is suspected to be an endophenotype of autism spectrum disorder (ASD). Reducing serotonin levels in the brain through modulation of serotonin transporter function may improve ASD symptoms. Methods: We analyzed behavior and gene expression to unveil the causal mechanism of ASD-relevant social deficits using serotonin transporter (Sert) knockout mice. Results: Social deficits were observed in both heterozygous knockout mice (HZ) and homozygous knockout mice (KO), but increases in general anxiety were only observed in KO mice. Two weeks of dietary restriction of the serotonin precursor tryptophan ameliorated both brain hyperserotonemia and ASD-relevant social deficits in Sert HZ and KO mice. The expression of rather distinct sets of genes was altered in Sert HZ and KO mice, and a substantial portion of these genes was also affected by tryptophan depletion. Tryptophan depletion in Sert HZ and KO mice was associated with alterations in the expression of genes involved in signal transduction pathways initiated by changes in extracellular serotonin or melatonin, a derivative of serotonin. Only expression of the AU015836 gene was altered in both Sert HZ and KO mice. AU015836 expression and ASD-relevant social deficits normalized after dietary tryptophan restriction. Conclusions: These findings reveal a Sert gene dose-dependent effect on brain hyperserotonemia and related behavioral sequelae in ASD and a possible therapeutic target to normalize brain hyperserotonemia and ASD-relevant social deficits. En ligne : https://dx.doi.org/10.1186/s13229-018-0243-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371
in Molecular Autism > 9 (2018) . - 60p.[article] Brain hyperserotonemia causes autism-relevant social deficits in mice [Texte imprimé et/ou numérique] / M. TANAKA, Auteur ; A. SATO, Auteur ; S. KASAI, Auteur ; Y. HAGINO, Auteur ; H. KOTAJIMA-MURAKAMI, Auteur ; H. KASHII, Auteur ; Y. TAKAMATSU, Auteur ; Y. NISHITO, Auteur ; M. INAGAKI, Auteur ; M. MIZUGUCHI, Auteur ; F. S. HALL, Auteur ; G. R. UHL, Auteur ; D. MURPHY, Auteur ; I. SORA, Auteur ; K. IKEDA, Auteur . - 60p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 60p.
Mots-clés : Autism spectrum disorder Heterozygous mice Serotonin transporter Tryptophan depletion Index. décimale : PER Périodiques Résumé : Background: Hyperserotonemia in the brain is suspected to be an endophenotype of autism spectrum disorder (ASD). Reducing serotonin levels in the brain through modulation of serotonin transporter function may improve ASD symptoms. Methods: We analyzed behavior and gene expression to unveil the causal mechanism of ASD-relevant social deficits using serotonin transporter (Sert) knockout mice. Results: Social deficits were observed in both heterozygous knockout mice (HZ) and homozygous knockout mice (KO), but increases in general anxiety were only observed in KO mice. Two weeks of dietary restriction of the serotonin precursor tryptophan ameliorated both brain hyperserotonemia and ASD-relevant social deficits in Sert HZ and KO mice. The expression of rather distinct sets of genes was altered in Sert HZ and KO mice, and a substantial portion of these genes was also affected by tryptophan depletion. Tryptophan depletion in Sert HZ and KO mice was associated with alterations in the expression of genes involved in signal transduction pathways initiated by changes in extracellular serotonin or melatonin, a derivative of serotonin. Only expression of the AU015836 gene was altered in both Sert HZ and KO mice. AU015836 expression and ASD-relevant social deficits normalized after dietary tryptophan restriction. Conclusions: These findings reveal a Sert gene dose-dependent effect on brain hyperserotonemia and related behavioral sequelae in ASD and a possible therapeutic target to normalize brain hyperserotonemia and ASD-relevant social deficits. En ligne : https://dx.doi.org/10.1186/s13229-018-0243-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 A pilot study of serotonergic modulation after long-term administration of oxytocin in autism spectrum disorder / Tetsu HIROSAWA in Autism Research, 10-5 (May 2017)
[article]
Titre : A pilot study of serotonergic modulation after long-term administration of oxytocin in autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Tetsu HIROSAWA, Auteur ; Mitsuru KIKUCHI, Auteur ; Yasuomi OUCHI, Auteur ; Tetsuya TAKAHASHI, Auteur ; Yuko YOSHIMURA, Auteur ; Hirotaka KOSAKA, Auteur ; Naoki FURUTANI, Auteur ; Hirotoshi HIRAISHI, Auteur ; Mina FUKAI, Auteur ; Masamichi YOKOKURA, Auteur ; Etsuji YOSHIKAWA, Auteur ; Tomoyasu BUNAI, Auteur ; Yoshio MINABE, Auteur Article en page(s) : p.821-828 Langues : Anglais (eng) Mots-clés : autism spectrum disorder oxytocin positron emission tomography serotonin transporter Index. décimale : PER Périodiques Résumé : Oxytocin (OT) and the serotonergic system putatively play important roles in autism spectrum disorder (ASD) etiology and symptoms, but no direct neurobiological evidence exists for long-term OT administration effects on the brain's serotonergic system. This pilot study examined 10 male participants with ASD who were administered OT intranasally for 8–10 weeks in an open-label, single-arm, nonrandomized, and uncontrolled manner. Positron emission tomography (PET) with a radiotracer (11C)?3-amino-4-(2-[(dimethylamino)methyl]phenylthio)benzonitrile (11C-DASB) was used before and after OT treatment. The binding potential of serotonin transporter (11C-DASB BPND) was then estimated. The main outcome measures were changes in 11C-DASB BPND and their correlation with changes in symptoms. ASD participants showed significantly elevated 11C-DASB BPND in the left inferior frontal gyrus extending to the left middle frontal gyrus. No significant correlation was found between the change in any clinical symptom and the change in 11C-DASB BPND. This report of a pilot study is the first describing long-term effects of OT on the brain's serotonin system in ASD. Additional randomized controlled studies must be conducted to confirm whether activation of the serotonergic system contributes to the prosocial effect of OT in people with ASD. En ligne : http://dx.doi.org/10.1002/aur.1761 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=307
in Autism Research > 10-5 (May 2017) . - p.821-828[article] A pilot study of serotonergic modulation after long-term administration of oxytocin in autism spectrum disorder [Texte imprimé et/ou numérique] / Tetsu HIROSAWA, Auteur ; Mitsuru KIKUCHI, Auteur ; Yasuomi OUCHI, Auteur ; Tetsuya TAKAHASHI, Auteur ; Yuko YOSHIMURA, Auteur ; Hirotaka KOSAKA, Auteur ; Naoki FURUTANI, Auteur ; Hirotoshi HIRAISHI, Auteur ; Mina FUKAI, Auteur ; Masamichi YOKOKURA, Auteur ; Etsuji YOSHIKAWA, Auteur ; Tomoyasu BUNAI, Auteur ; Yoshio MINABE, Auteur . - p.821-828.
Langues : Anglais (eng)
in Autism Research > 10-5 (May 2017) . - p.821-828
Mots-clés : autism spectrum disorder oxytocin positron emission tomography serotonin transporter Index. décimale : PER Périodiques Résumé : Oxytocin (OT) and the serotonergic system putatively play important roles in autism spectrum disorder (ASD) etiology and symptoms, but no direct neurobiological evidence exists for long-term OT administration effects on the brain's serotonergic system. This pilot study examined 10 male participants with ASD who were administered OT intranasally for 8–10 weeks in an open-label, single-arm, nonrandomized, and uncontrolled manner. Positron emission tomography (PET) with a radiotracer (11C)?3-amino-4-(2-[(dimethylamino)methyl]phenylthio)benzonitrile (11C-DASB) was used before and after OT treatment. The binding potential of serotonin transporter (11C-DASB BPND) was then estimated. The main outcome measures were changes in 11C-DASB BPND and their correlation with changes in symptoms. ASD participants showed significantly elevated 11C-DASB BPND in the left inferior frontal gyrus extending to the left middle frontal gyrus. No significant correlation was found between the change in any clinical symptom and the change in 11C-DASB BPND. This report of a pilot study is the first describing long-term effects of OT on the brain's serotonin system in ASD. Additional randomized controlled studies must be conducted to confirm whether activation of the serotonergic system contributes to the prosocial effect of OT in people with ASD. En ligne : http://dx.doi.org/10.1002/aur.1761 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=307