Centre d'Information et de documentation du CRA Rhône-Alpes
CRA
Informations pratiques
-
Adresse
Centre d'information et de documentation
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexHoraires
Lundi au Vendredi
9h00-12h00 13h30-16h00Contact
Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Résultat de la recherche
16 recherche sur le mot-clé 'Neuroinflammation'
Affiner la recherche Générer le flux rss de la recherche
Partager le résultat de cette recherche Faire une suggestion
Annual Research Review: The neuroinflammation hypothesis for stress and psychopathology in children – developmental psychoneuroimmunology / Thomas G. O'CONNOR in Journal of Child Psychology and Psychiatry, 55-6 (June 2014)
[article]
Titre : Annual Research Review: The neuroinflammation hypothesis for stress and psychopathology in children – developmental psychoneuroimmunology Type de document : Texte imprimé et/ou numérique Auteurs : Thomas G. O'CONNOR, Auteur ; Jan A. MOYNIHAN, Auteur ; Mary T. CASERTA, Auteur Année de publication : 2014 Article en page(s) : p.615-631 Langues : Anglais (eng) Mots-clés : Immunology psychoneuroimmunology neuroinflammation stress developmental psychopathology Index. décimale : PER Périodiques Résumé : Abstract Experimental animal and adult human data suggest that stress exposure is associated with alterations in immune system function that may underlie increased susceptibility to disease and behavioral disorders. The implications of these data for child psychology and psychiatry are not yet clear. The current review seeks to distil and translate the relevant animal and adult human work to children to advance a developmental model of psychoneuroimmunology. In addition to reviewing key specific findings, we consider biological/conceptual models and technical aspects of psychoneuroimmunology work in pediatric populations, and outline the rationales and advantages of integrating hypotheses concerning neuroinflammation in developmental studies of psychopathology. En ligne : http://dx.doi.org/10.1111/jcpp.12187 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=234
in Journal of Child Psychology and Psychiatry > 55-6 (June 2014) . - p.615-631[article] Annual Research Review: The neuroinflammation hypothesis for stress and psychopathology in children – developmental psychoneuroimmunology [Texte imprimé et/ou numérique] / Thomas G. O'CONNOR, Auteur ; Jan A. MOYNIHAN, Auteur ; Mary T. CASERTA, Auteur . - 2014 . - p.615-631.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 55-6 (June 2014) . - p.615-631
Mots-clés : Immunology psychoneuroimmunology neuroinflammation stress developmental psychopathology Index. décimale : PER Périodiques Résumé : Abstract Experimental animal and adult human data suggest that stress exposure is associated with alterations in immune system function that may underlie increased susceptibility to disease and behavioral disorders. The implications of these data for child psychology and psychiatry are not yet clear. The current review seeks to distil and translate the relevant animal and adult human work to children to advance a developmental model of psychoneuroimmunology. In addition to reviewing key specific findings, we consider biological/conceptual models and technical aspects of psychoneuroimmunology work in pediatric populations, and outline the rationales and advantages of integrating hypotheses concerning neuroinflammation in developmental studies of psychopathology. En ligne : http://dx.doi.org/10.1111/jcpp.12187 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=234 Can Neuroinflammation Influence the Development of Autism Spectrum Disorders? / Carlos A. PARDO-VIILLAMIZAR
Titre : Can Neuroinflammation Influence the Development of Autism Spectrum Disorders? Type de document : Texte imprimé et/ou numérique Auteurs : Carlos A. PARDO-VIILLAMIZAR, Auteur Année de publication : 2008 Importance : p.329-346 Langues : Anglais (eng) Mots-clés : Neuroimmunité Neuroinflammation Neurodéveloppement Astrocyte Microglie Neuroglie Cytokine Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=704 Can Neuroinflammation Influence the Development of Autism Spectrum Disorders? [Texte imprimé et/ou numérique] / Carlos A. PARDO-VIILLAMIZAR, Auteur . - 2008 . - p.329-346.
Langues : Anglais (eng)
Mots-clés : Neuroimmunité Neuroinflammation Neurodéveloppement Astrocyte Microglie Neuroglie Cytokine Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=704 Exemplaires
Code-barres Cote Support Localisation Section Disponibilité aucun exemplaire A pilot study of high-dose intravenous immunoglobulin 5% for autism: Impact on autism spectrum and markers of neuroinflammation / I. R. MELAMED in Autism Research, 11-3 (March 2018)
[article]
Titre : A pilot study of high-dose intravenous immunoglobulin 5% for autism: Impact on autism spectrum and markers of neuroinflammation Type de document : Texte imprimé et/ou numérique Auteurs : I. R. MELAMED, Auteur ; M. HEFFRON, Auteur ; A. TESTORI, Auteur ; K. LIPE, Auteur Article en page(s) : p.421-433 Langues : Anglais (eng) Mots-clés : autism spectrum disorder epigenetic innate immunity intravenous immunoglobulin neuroinflammation Index. décimale : PER Périodiques Résumé : Research has shown that a subset of the autism spectrum disorder (ASD) population presents with immune dysregulation. To explore this topic further, we investigated the efficacy and tolerability of intravenous immunoglobulin (IVIG) infusion in children with ASD. In this study, participants were recruited based on a diagnosis of autistic disorder, Asperger's disorder, or pervasive developmental disorder not otherwise specified. Participants also showed evidence of immune dysfunction based on abnormal levels of specific biomarkers, including CD40 ligand (CD154), lymphocyte stimulation, and T or B cell dysfunction. Of 17 screened patients, 14 completed the trial and received IVIG treatment (1 g/kg dose) for ten 21-day treatment cycles. The primary endpoint was disease improvement assessed using standardized cognitive and behavioral tests (Children's Communication Checklist [CCC-2], Social Responsiveness Scale [SRS], Aberrant Behavior Checklist [ABC], Clinical Global Impressions-Severity [CGI-S] and -Improvement [CGI-I], Autism Diagnostic Observation Schedule [ADOS], and Peabody Picture Vocabulary Test [PPVT]). Secondary endpoints included experimental biomarkers such as CD154, toll-like receptor-4, memory B cells, FOXP3, and lymphocyte stimulation. Significant improvements from baseline to study endpoint were observed in several subscales of the CCC-2, SRS, CGI-I, CGI-S, and ADOS, including Associated Maladaptive Behaviors (P = .043), Reciprocal Social Interaction (P = .015), Communication (P < .001), and Stereotyped Behaviors and Repetitive Interests (P = .013). Statistically significant reductions were also seen in numerous secondary outcomes of immunological biomarkers indicative of neuroinflammation. IVIG was well tolerated; no subjects withdrew due to an adverse event, and clinical data showed no evidence of thromboembolic events. Autism Res 2018, 11: 421-433. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Since research has demonstrated a link between autism spectrum disorder (ASD) and immune dysfunction, this study investigated the efficacy and tolerability of intravenous immunoglobulin (IVIG) infusion in children with ASD. Fourteen patients received IVIG treatment and were assessed using standardized cognitive and behavioral tests. Following treatment with IVIG, significant improvement was observed across several subscales of the clinical tests and significant reductions were seen in the markers of neuroinflammation. These data suggest that inflammatory etiologies may play a role in select cases of autism, and IVIG treatment may exert a positive impact on behaviors and markers of inflammation in ASD. En ligne : http://dx.doi.org/10.1002/aur.1906 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=352
in Autism Research > 11-3 (March 2018) . - p.421-433[article] A pilot study of high-dose intravenous immunoglobulin 5% for autism: Impact on autism spectrum and markers of neuroinflammation [Texte imprimé et/ou numérique] / I. R. MELAMED, Auteur ; M. HEFFRON, Auteur ; A. TESTORI, Auteur ; K. LIPE, Auteur . - p.421-433.
Langues : Anglais (eng)
in Autism Research > 11-3 (March 2018) . - p.421-433
Mots-clés : autism spectrum disorder epigenetic innate immunity intravenous immunoglobulin neuroinflammation Index. décimale : PER Périodiques Résumé : Research has shown that a subset of the autism spectrum disorder (ASD) population presents with immune dysregulation. To explore this topic further, we investigated the efficacy and tolerability of intravenous immunoglobulin (IVIG) infusion in children with ASD. In this study, participants were recruited based on a diagnosis of autistic disorder, Asperger's disorder, or pervasive developmental disorder not otherwise specified. Participants also showed evidence of immune dysfunction based on abnormal levels of specific biomarkers, including CD40 ligand (CD154), lymphocyte stimulation, and T or B cell dysfunction. Of 17 screened patients, 14 completed the trial and received IVIG treatment (1 g/kg dose) for ten 21-day treatment cycles. The primary endpoint was disease improvement assessed using standardized cognitive and behavioral tests (Children's Communication Checklist [CCC-2], Social Responsiveness Scale [SRS], Aberrant Behavior Checklist [ABC], Clinical Global Impressions-Severity [CGI-S] and -Improvement [CGI-I], Autism Diagnostic Observation Schedule [ADOS], and Peabody Picture Vocabulary Test [PPVT]). Secondary endpoints included experimental biomarkers such as CD154, toll-like receptor-4, memory B cells, FOXP3, and lymphocyte stimulation. Significant improvements from baseline to study endpoint were observed in several subscales of the CCC-2, SRS, CGI-I, CGI-S, and ADOS, including Associated Maladaptive Behaviors (P = .043), Reciprocal Social Interaction (P = .015), Communication (P < .001), and Stereotyped Behaviors and Repetitive Interests (P = .013). Statistically significant reductions were also seen in numerous secondary outcomes of immunological biomarkers indicative of neuroinflammation. IVIG was well tolerated; no subjects withdrew due to an adverse event, and clinical data showed no evidence of thromboembolic events. Autism Res 2018, 11: 421-433. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Since research has demonstrated a link between autism spectrum disorder (ASD) and immune dysfunction, this study investigated the efficacy and tolerability of intravenous immunoglobulin (IVIG) infusion in children with ASD. Fourteen patients received IVIG treatment and were assessed using standardized cognitive and behavioral tests. Following treatment with IVIG, significant improvement was observed across several subscales of the clinical tests and significant reductions were seen in the markers of neuroinflammation. These data suggest that inflammatory etiologies may play a role in select cases of autism, and IVIG treatment may exert a positive impact on behaviors and markers of inflammation in ASD. En ligne : http://dx.doi.org/10.1002/aur.1906 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=352 Blood-brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders / M. FIORENTINO in Molecular Autism, 7 (2016)
[article]
Titre : Blood-brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders Type de document : Texte imprimé et/ou numérique Auteurs : M. FIORENTINO, Auteur ; A. SAPONE, Auteur ; S. SENGER, Auteur ; S. S. CAMHI, Auteur ; S. M. KADZIELSKI, Auteur ; Timothy M. BUIE, Auteur ; D. L. KELLY, Auteur ; N. CASCELLA, Auteur ; A. FASANO, Auteur Article en page(s) : 49p. Langues : Anglais (eng) Mots-clés : Adolescent Adult Autism Spectrum Disorder/genetics/immunology/metabolism/pathology Biopsy Blood-Brain Barrier/immunology/metabolism/pathology Case-Control Studies Cerebellum/immunology/metabolism/pathology Cerebral Cortex/immunology/metabolism/pathology Child Child, Preschool Claudin-3/genetics/immunology Claudin-5/genetics/immunology Claudins/genetics/immunology DNA-Binding Proteins/genetics/immunology Duodenum/immunology/metabolism/pathology Female Gene Expression Humans Interleukin-1beta/genetics/immunology Interleukin-8/genetics/immunology MARVEL Domain Containing 2 Protein/genetics/immunology Male Matrix Metalloproteinase 9/genetics/immunology Middle Aged Permeability Schizophrenia/genetics/immunology/metabolism/pathology Tight Junctions/immunology/metabolism/pathology Autism spectrum disorders Blood-brain barrier Duodenal biopsies Gut permeability Gut-brain axis Neuroinflammation Postmortem brain Schizophrenia Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASD) are complex conditions whose pathogenesis may be attributed to gene-environment interactions. There are no definitive mechanisms explaining how environmental triggers can lead to ASD although the involvement of inflammation and immunity has been suggested. Inappropriate antigen trafficking through an impaired intestinal barrier, followed by passage of these antigens or immune-activated complexes through a permissive blood-brain barrier (BBB), can be part of the chain of events leading to these disorders. Our goal was to investigate whether an altered BBB and gut permeability is part of the pathophysiology of ASD. METHODS: Postmortem cerebral cortex and cerebellum tissues from ASD, schizophrenia (SCZ), and healthy subjects (HC) and duodenal biopsies from ASD and HC were analyzed for gene and protein expression profiles. Tight junctions and other key molecules associated with the neurovascular unit integrity and function and neuroinflammation were investigated. RESULTS: Claudin (CLDN)-5 and -12 were increased in the ASD cortex and cerebellum. CLDN-3, tricellulin, and MMP-9 were higher in the ASD cortex. IL-8, tPA, and IBA-1 were downregulated in SCZ cortex; IL-1b was increased in the SCZ cerebellum. Differences between SCZ and ASD were observed for most of the genes analyzed in both brain areas. CLDN-5 protein was increased in ASD cortex and cerebellum, while CLDN-12 appeared reduced in both ASD and SCZ cortexes. In the intestine, 75% of the ASD samples analyzed had reduced expression of barrier-forming TJ components (CLDN-1, OCLN, TRIC), whereas 66% had increased pore-forming CLDNs (CLDN-2, -10, -15) compared to controls. CONCLUSIONS: In the ASD brain, there is an altered expression of genes associated with BBB integrity coupled with increased neuroinflammation and possibly impaired gut barrier integrity. While these findings seem to be specific for ASD, the possibility of more distinct SCZ subgroups should be explored with additional studies. En ligne : http://dx.doi.org/10.1186/s13229-016-0110-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328
in Molecular Autism > 7 (2016) . - 49p.[article] Blood-brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders [Texte imprimé et/ou numérique] / M. FIORENTINO, Auteur ; A. SAPONE, Auteur ; S. SENGER, Auteur ; S. S. CAMHI, Auteur ; S. M. KADZIELSKI, Auteur ; Timothy M. BUIE, Auteur ; D. L. KELLY, Auteur ; N. CASCELLA, Auteur ; A. FASANO, Auteur . - 49p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 49p.
Mots-clés : Adolescent Adult Autism Spectrum Disorder/genetics/immunology/metabolism/pathology Biopsy Blood-Brain Barrier/immunology/metabolism/pathology Case-Control Studies Cerebellum/immunology/metabolism/pathology Cerebral Cortex/immunology/metabolism/pathology Child Child, Preschool Claudin-3/genetics/immunology Claudin-5/genetics/immunology Claudins/genetics/immunology DNA-Binding Proteins/genetics/immunology Duodenum/immunology/metabolism/pathology Female Gene Expression Humans Interleukin-1beta/genetics/immunology Interleukin-8/genetics/immunology MARVEL Domain Containing 2 Protein/genetics/immunology Male Matrix Metalloproteinase 9/genetics/immunology Middle Aged Permeability Schizophrenia/genetics/immunology/metabolism/pathology Tight Junctions/immunology/metabolism/pathology Autism spectrum disorders Blood-brain barrier Duodenal biopsies Gut permeability Gut-brain axis Neuroinflammation Postmortem brain Schizophrenia Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASD) are complex conditions whose pathogenesis may be attributed to gene-environment interactions. There are no definitive mechanisms explaining how environmental triggers can lead to ASD although the involvement of inflammation and immunity has been suggested. Inappropriate antigen trafficking through an impaired intestinal barrier, followed by passage of these antigens or immune-activated complexes through a permissive blood-brain barrier (BBB), can be part of the chain of events leading to these disorders. Our goal was to investigate whether an altered BBB and gut permeability is part of the pathophysiology of ASD. METHODS: Postmortem cerebral cortex and cerebellum tissues from ASD, schizophrenia (SCZ), and healthy subjects (HC) and duodenal biopsies from ASD and HC were analyzed for gene and protein expression profiles. Tight junctions and other key molecules associated with the neurovascular unit integrity and function and neuroinflammation were investigated. RESULTS: Claudin (CLDN)-5 and -12 were increased in the ASD cortex and cerebellum. CLDN-3, tricellulin, and MMP-9 were higher in the ASD cortex. IL-8, tPA, and IBA-1 were downregulated in SCZ cortex; IL-1b was increased in the SCZ cerebellum. Differences between SCZ and ASD were observed for most of the genes analyzed in both brain areas. CLDN-5 protein was increased in ASD cortex and cerebellum, while CLDN-12 appeared reduced in both ASD and SCZ cortexes. In the intestine, 75% of the ASD samples analyzed had reduced expression of barrier-forming TJ components (CLDN-1, OCLN, TRIC), whereas 66% had increased pore-forming CLDNs (CLDN-2, -10, -15) compared to controls. CONCLUSIONS: In the ASD brain, there is an altered expression of genes associated with BBB integrity coupled with increased neuroinflammation and possibly impaired gut barrier integrity. While these findings seem to be specific for ASD, the possibility of more distinct SCZ subgroups should be explored with additional studies. En ligne : http://dx.doi.org/10.1186/s13229-016-0110-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328 Germline nuclear-predominant Pten murine model exhibits impaired social and perseverative behavior, microglial activation, and increased oxytocinergic activity / N. SARN in Molecular Autism, 12 (2021)
[article]
Titre : Germline nuclear-predominant Pten murine model exhibits impaired social and perseverative behavior, microglial activation, and increased oxytocinergic activity Type de document : Texte imprimé et/ou numérique Auteurs : N. SARN, Auteur ; S. THACKER, Auteur ; H. LEE, Auteur ; C. ENG, Auteur Article en page(s) : 41 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Complement Microglia Mouse model Neurodegeneration Neuroinflammation Oxytocin PTEN mutation Social impairment Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) has a strong genetic etiology. Germline mutation in the tumor suppressor gene PTEN is one of the best described monogenic risk cases for ASD. Animal modeling of cell-specific Pten loss or mutation has provided insight into how disruptions to the function of PTEN affect neurodevelopment, neurobiology, and social behavior. As such, there is a growing need to understand more about how various aspects of PTEN activity and cell-compartment-specific functions, contribute to certain neurological or behavior phenotypes. METHODS: To understand more about the relationship between Pten localization and downstream effects on neurophenotypes, we generated the nuclear-predominant Pten(Y68H/+) mouse, which is identical to the genotype of some PTEN-ASD individuals. We subjected the Pten(Y68H/+) mouse to morphological and behavioral phenotyping, including the three-chamber sociability, open field, rotarod, and marble burying tests. We subsequently performed in vivo and in vitro cellular phenotyping and concluded the work with a transcriptomic survey of the Pten(Y68H/+) cortex, which profiled gene expression. RESULTS: We observe a significant increase in P-Akt downstream of canonical Pten signaling, macrocephaly, decreased sociability, decreased preference for novel social stimuli, increased repetitive behavior, and increased thigmotaxis in Pten(Y68H/+) six-week-old (P40) mice. In addition, we found significant microglial activation with increased expression of complement and neuroinflammatory proteins in vivo and in vitro accompanied by enhanced phagocytosis. These observations were subsequently validated with RNA-seq and qRT-PCR, which revealed overexpression of many genes involved in neuroinflammation and neuronal function, including oxytocin. Oxytocin transcript was fivefold overexpressed (P?=?0.0018), and oxytocin protein was strongly overexpressed in the Pten(Y68H/+) hypothalamus. CONCLUSIONS: The nuclear-predominant Pten(Y68H/+) model has clarified that Pten dysfunction links to microglial pathology and this associates with increased Akt signaling. We also demonstrate that Pten dysfunction associates with changes in the oxytocin system, an important connection between a prominent ASD risk gene and a potent neuroendocrine regulator of social behavior. These cellular and molecular pathologies may related to the observed changes in social behavior. Ultimately, the findings from this work may reveal important biomarkers and/or novel therapeutic modalities that could be explored in individuals with germline mutations in PTEN with ASD. En ligne : http://dx.doi.org/10.1186/s13229-021-00448-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459
in Molecular Autism > 12 (2021) . - 41 p.[article] Germline nuclear-predominant Pten murine model exhibits impaired social and perseverative behavior, microglial activation, and increased oxytocinergic activity [Texte imprimé et/ou numérique] / N. SARN, Auteur ; S. THACKER, Auteur ; H. LEE, Auteur ; C. ENG, Auteur . - 41 p.
Langues : Anglais (eng)
in Molecular Autism > 12 (2021) . - 41 p.
Mots-clés : Autism spectrum disorder Complement Microglia Mouse model Neurodegeneration Neuroinflammation Oxytocin PTEN mutation Social impairment Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) has a strong genetic etiology. Germline mutation in the tumor suppressor gene PTEN is one of the best described monogenic risk cases for ASD. Animal modeling of cell-specific Pten loss or mutation has provided insight into how disruptions to the function of PTEN affect neurodevelopment, neurobiology, and social behavior. As such, there is a growing need to understand more about how various aspects of PTEN activity and cell-compartment-specific functions, contribute to certain neurological or behavior phenotypes. METHODS: To understand more about the relationship between Pten localization and downstream effects on neurophenotypes, we generated the nuclear-predominant Pten(Y68H/+) mouse, which is identical to the genotype of some PTEN-ASD individuals. We subjected the Pten(Y68H/+) mouse to morphological and behavioral phenotyping, including the three-chamber sociability, open field, rotarod, and marble burying tests. We subsequently performed in vivo and in vitro cellular phenotyping and concluded the work with a transcriptomic survey of the Pten(Y68H/+) cortex, which profiled gene expression. RESULTS: We observe a significant increase in P-Akt downstream of canonical Pten signaling, macrocephaly, decreased sociability, decreased preference for novel social stimuli, increased repetitive behavior, and increased thigmotaxis in Pten(Y68H/+) six-week-old (P40) mice. In addition, we found significant microglial activation with increased expression of complement and neuroinflammatory proteins in vivo and in vitro accompanied by enhanced phagocytosis. These observations were subsequently validated with RNA-seq and qRT-PCR, which revealed overexpression of many genes involved in neuroinflammation and neuronal function, including oxytocin. Oxytocin transcript was fivefold overexpressed (P?=?0.0018), and oxytocin protein was strongly overexpressed in the Pten(Y68H/+) hypothalamus. CONCLUSIONS: The nuclear-predominant Pten(Y68H/+) model has clarified that Pten dysfunction links to microglial pathology and this associates with increased Akt signaling. We also demonstrate that Pten dysfunction associates with changes in the oxytocin system, an important connection between a prominent ASD risk gene and a potent neuroendocrine regulator of social behavior. These cellular and molecular pathologies may related to the observed changes in social behavior. Ultimately, the findings from this work may reveal important biomarkers and/or novel therapeutic modalities that could be explored in individuals with germline mutations in PTEN with ASD. En ligne : http://dx.doi.org/10.1186/s13229-021-00448-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459 Integrated genome-wide Alu methylation and transcriptome profiling analyses reveal novel epigenetic regulatory networks associated with autism spectrum disorder / T. SAELIW in Molecular Autism, 9 (2018)
PermalinkNeuroinflammatory Gene Expression Alterations in Anterior Cingulate Cortical White and Gray Matter of Males With Autism Spectrum Disorder / Aubrey N. SCIARA in Autism Research, 13-6 (June 2020)
PermalinkA pilot open-label trial of minocycline in patients with autism and regressive features / Carlos A. PARDO in Journal of Neurodevelopmental Disorders, 5-1 (December 2013)
PermalinkAlterations in plasma cytokine levels in chinese children with autism spectrum disorder / C. C. HU in Autism Research, 11-7 (July 2018)
PermalinkAltered kynurenine pathway metabolism in autism: Implication for immune-induced glutamatergic activity / Chai K. LIM in Autism Research, 9-6 (June 2016)
Permalink