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Faire une suggestionRole for antibodies in altering behavior and movement / Jane E. LIBBEY in Autism Research, 3-4 (August 2010)
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Titre : Role for antibodies in altering behavior and movement Type de document : texte imprimé Auteurs : Jane E. LIBBEY, Auteur ; Robert S. FUJINAMI, Auteur Année de publication : 2010 Article en page(s) : p.147-152 Langues : Anglais (eng) Mots-clés : antibody autism chorea humoral-immunity systemic-lupus-erythematosus Index. décimale : PER Périodiques Résumé : At the past meeting of INSAR, the role of autoimmunity was discussed in an educational session. This article summarizes this discussion. In immune-mediated diseases, antibodies can contribute to the pathogenesis of the disease and are sometimes the force that drives the disease process. This concept has not been established for autism. In autoimmune diseases, such as systemic lupus erythematosus (SLE), antibodies are found to react with double-stranded DNA. These antibodies also cross-react with N-methyl-D aspartate receptors. Many SLE patients suffer neurologic syndromes of the central nervous system (CNS). Similarly individuals infected with Group A streptococcus (GAS) have antibodies against the GAS carbohydrate, which cross-react with tubulin and lysoganglioside GM1 on neurons. During the acute stage of infection, GAS-infected patients develop Syndenham chorea where the disease process is driven in part by these cross-reactive antibodies. As the antibody levels decrease, the clinical features of Syndenham chorea resolve. In these two immune-mediated diseases, antibodies clearly play a role in the pathogenesis of the diseases. There are reports that mothers of individuals with autism have antibodies that react with brain proteins and when these antibodies are passively transferred to pregnant non-human primates or rodents the offspring has behavioral and nervous system changes. It is still not clear whether the antibodies found in mothers of individuals with autism actually play a role in the disease. More studies need to be performed to identify the proteins recognized by the antibodies and to determine how these could affect development, behavior and changes within the CNS. En ligne : http://dx.doi.org/10.1002/aur.144 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=109
in Autism Research > 3-4 (August 2010) . - p.147-152[article] Role for antibodies in altering behavior and movement [texte imprimé] / Jane E. LIBBEY, Auteur ; Robert S. FUJINAMI, Auteur . - 2010 . - p.147-152.
Langues : Anglais (eng)
in Autism Research > 3-4 (August 2010) . - p.147-152
Mots-clés : antibody autism chorea humoral-immunity systemic-lupus-erythematosus Index. décimale : PER Périodiques Résumé : At the past meeting of INSAR, the role of autoimmunity was discussed in an educational session. This article summarizes this discussion. In immune-mediated diseases, antibodies can contribute to the pathogenesis of the disease and are sometimes the force that drives the disease process. This concept has not been established for autism. In autoimmune diseases, such as systemic lupus erythematosus (SLE), antibodies are found to react with double-stranded DNA. These antibodies also cross-react with N-methyl-D aspartate receptors. Many SLE patients suffer neurologic syndromes of the central nervous system (CNS). Similarly individuals infected with Group A streptococcus (GAS) have antibodies against the GAS carbohydrate, which cross-react with tubulin and lysoganglioside GM1 on neurons. During the acute stage of infection, GAS-infected patients develop Syndenham chorea where the disease process is driven in part by these cross-reactive antibodies. As the antibody levels decrease, the clinical features of Syndenham chorea resolve. In these two immune-mediated diseases, antibodies clearly play a role in the pathogenesis of the diseases. There are reports that mothers of individuals with autism have antibodies that react with brain proteins and when these antibodies are passively transferred to pregnant non-human primates or rodents the offspring has behavioral and nervous system changes. It is still not clear whether the antibodies found in mothers of individuals with autism actually play a role in the disease. More studies need to be performed to identify the proteins recognized by the antibodies and to determine how these could affect development, behavior and changes within the CNS. En ligne : http://dx.doi.org/10.1002/aur.144 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=109 Challenges in researching the immune pathways between early life adversity and psychopathology / Brie REID in Development and Psychopathology, 32-5 (December 2020)
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Titre : Challenges in researching the immune pathways between early life adversity and psychopathology Type de document : texte imprimé Auteurs : Brie REID, Auteur ; Andrea DANESE, Auteur Article en page(s) : p.1597-1624 Langues : Anglais (eng) Mots-clés : Biomarkers Child Humans Inflammation *Psychopathology Risk Factors *Stress, Psychological *childhood adversity *immunity *inflammation *maltreatment *psychiatric disorders Index. décimale : PER Périodiques Résumé : Exposure to childhood adversity is a critical risk factor for the development of psychopathology. A growing field of research examines how exposure to childhood adversity is translated into biological risk for psychopathology through alterations in immune system functioning, most notably heightened levels of inflammation biomarkers. Though our knowledge about how childhood adversity can instantiate biological risk for psychopathology is growing, there remain many challenges and gaps in the field to understand how inflammation from childhood adversity contributes to psychopathology. This paper reviews research on the inflammatory outcomes arising from childhood adversity and presents four major challenges that future research must address: (a) the measurement of childhood adversity, (b) the measurement of inflammation, (c) the identification of mediators between childhood adversity and inflammation, and (d) the identification of moderators of inflammatory outcomes following childhood adversity. We discuss synergies and inconsistencies in the literature to summarize the current understanding of the association between childhood adversity, a proinflammatory phenotype, and the biological risk for psychopathology. We discuss the clinical implications of the inflammatory links between childhood adversity and psychopathology, including possibilities for intervention. Finally, this review conclude by delineates future directions for research, including issues of how best to detect, prevent, and understand these "hidden wounds" of childhood adversity. En ligne : http://dx.doi.org/10.1017/s0954579420001157 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437
in Development and Psychopathology > 32-5 (December 2020) . - p.1597-1624[article] Challenges in researching the immune pathways between early life adversity and psychopathology [texte imprimé] / Brie REID, Auteur ; Andrea DANESE, Auteur . - p.1597-1624.
Langues : Anglais (eng)
in Development and Psychopathology > 32-5 (December 2020) . - p.1597-1624
Mots-clés : Biomarkers Child Humans Inflammation *Psychopathology Risk Factors *Stress, Psychological *childhood adversity *immunity *inflammation *maltreatment *psychiatric disorders Index. décimale : PER Périodiques Résumé : Exposure to childhood adversity is a critical risk factor for the development of psychopathology. A growing field of research examines how exposure to childhood adversity is translated into biological risk for psychopathology through alterations in immune system functioning, most notably heightened levels of inflammation biomarkers. Though our knowledge about how childhood adversity can instantiate biological risk for psychopathology is growing, there remain many challenges and gaps in the field to understand how inflammation from childhood adversity contributes to psychopathology. This paper reviews research on the inflammatory outcomes arising from childhood adversity and presents four major challenges that future research must address: (a) the measurement of childhood adversity, (b) the measurement of inflammation, (c) the identification of mediators between childhood adversity and inflammation, and (d) the identification of moderators of inflammatory outcomes following childhood adversity. We discuss synergies and inconsistencies in the literature to summarize the current understanding of the association between childhood adversity, a proinflammatory phenotype, and the biological risk for psychopathology. We discuss the clinical implications of the inflammatory links between childhood adversity and psychopathology, including possibilities for intervention. Finally, this review conclude by delineates future directions for research, including issues of how best to detect, prevent, and understand these "hidden wounds" of childhood adversity. En ligne : http://dx.doi.org/10.1017/s0954579420001157 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437 Frequency of Dendritic Cells and Their Expression of Costimulatory Molecules in Children with Autism Spectrum Disorders / Khaled SAAD in Journal of Autism and Developmental Disorders, 47-9 (September 2017)
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Titre : Frequency of Dendritic Cells and Their Expression of Costimulatory Molecules in Children with Autism Spectrum Disorders Type de document : texte imprimé Auteurs : Khaled SAAD, Auteur ; Asmaa M. ZAHRAN, Auteur ; Khalid I. ELSAYH, Auteur ; Ahmed A. ABDEL-RAHMAN, Auteur ; Abdulrahman A. AL-ATRAM, Auteur ; Almontaser HUSSEIN, Auteur ; Yasmin G. EL-GENDY, Auteur Article en page(s) : p.2671-2678 Langues : Anglais (eng) Mots-clés : Autism spectrum disorders Dendritic cells Innate immunity Children Index. décimale : PER Périodiques Résumé : The aim of our study was to evaluate the frequencies of myeloid dendritic cells (mDCs) and plasmacytoid dendritic cells (pDCs) in children with ASD. Subjects were 32 children with ASD and 30 healthy children as controls. The numbers of mDCs and pDCs and the expression of CD86 and CD80 on the entire DCs were detected by flow cytometry. ASD children had significantly higher percentages of mDCs and pDCs when compared to controls. We found significant inverse relationships between serum 25-hydroxyvitamin D levels and the frequencies of mDCs and pDCs in autistic children. Our data suggested that DCs could play a role in the clinical course of ASD. The relationship of DCs to immune disorders in ASD remains to be determined. En ligne : https://doi.org/10.1007/s10803-017-3190-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=315
in Journal of Autism and Developmental Disorders > 47-9 (September 2017) . - p.2671-2678[article] Frequency of Dendritic Cells and Their Expression of Costimulatory Molecules in Children with Autism Spectrum Disorders [texte imprimé] / Khaled SAAD, Auteur ; Asmaa M. ZAHRAN, Auteur ; Khalid I. ELSAYH, Auteur ; Ahmed A. ABDEL-RAHMAN, Auteur ; Abdulrahman A. AL-ATRAM, Auteur ; Almontaser HUSSEIN, Auteur ; Yasmin G. EL-GENDY, Auteur . - p.2671-2678.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 47-9 (September 2017) . - p.2671-2678
Mots-clés : Autism spectrum disorders Dendritic cells Innate immunity Children Index. décimale : PER Périodiques Résumé : The aim of our study was to evaluate the frequencies of myeloid dendritic cells (mDCs) and plasmacytoid dendritic cells (pDCs) in children with ASD. Subjects were 32 children with ASD and 30 healthy children as controls. The numbers of mDCs and pDCs and the expression of CD86 and CD80 on the entire DCs were detected by flow cytometry. ASD children had significantly higher percentages of mDCs and pDCs when compared to controls. We found significant inverse relationships between serum 25-hydroxyvitamin D levels and the frequencies of mDCs and pDCs in autistic children. Our data suggested that DCs could play a role in the clinical course of ASD. The relationship of DCs to immune disorders in ASD remains to be determined. En ligne : https://doi.org/10.1007/s10803-017-3190-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=315 From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition / Adam M.H. YOUNG in Molecular Autism, 7 (2016)
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Titre : From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition Type de document : texte imprimé Auteurs : Adam M.H. YOUNG, Auteur ; Bhismadev CHAKRABARTI, Auteur ; David ROBERTS, Auteur ; Meng-Chuan LAI, Auteur ; John SUCKLING, Auteur ; Simon BARON-COHEN, Auteur Article en page(s) : 9p. Langues : Anglais (eng) Mots-clés : Amniotic Fluid/chemistry Animals Antigens, Surface/immunology Autism Spectrum Disorder/genetics/immunology/pathology Autoantibodies/analysis Body Fluids/chemistry Brain/embryology/immunology/pathology Brain Chemistry Chemokines/analysis Cytokines/analysis Female Glutamic Acid/metabolism HLA Antigens/immunology Haplorhini Humans Immunity, Maternally-Acquired Inflammation Inflammation Mediators/analysis Lipopolysaccharides/blood Maternal-Fetal Exchange Mice Nerve Tissue Proteins/immunology Neuroglia/physiology Neuroimaging Pregnancy Pregnancy Complications, Infectious/blood Prenatal Exposure Delayed Effects Signal Transduction Autism Brain NF-kappaB Index. décimale : PER Périodiques Résumé : Growing evidence points toward a critical role for early (prenatal) atypical neurodevelopmental processes in the aetiology of autism spectrum condition (ASC). One such process that could impact early neural development is inflammation. We review the evidence for atypical expression of molecular markers in the amniotic fluid, serum, cerebrospinal fluid (CSF), and the brain parenchyma that suggest a role for inflammation in the emergence of ASC. This is complemented with a number of neuroimaging and neuropathological studies describing microglial activation. Implications for treatment are discussed. En ligne : http://dx.doi.org/10.1186/s13229-016-0068-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329
in Molecular Autism > 7 (2016) . - 9p.[article] From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition [texte imprimé] / Adam M.H. YOUNG, Auteur ; Bhismadev CHAKRABARTI, Auteur ; David ROBERTS, Auteur ; Meng-Chuan LAI, Auteur ; John SUCKLING, Auteur ; Simon BARON-COHEN, Auteur . - 9p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 9p.Hypovitaminosis D in persons with Down syndrome and autism spectrum disorder / Natalie K. BOYD in Journal of Neurodevelopmental Disorders, 15 (2023)
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Titre : Hypovitaminosis D in persons with Down syndrome and autism spectrum disorder Type de document : texte imprimé Auteurs : Natalie K. BOYD, Auteur ; Julia NGUYEN, Auteur ; Mellad M. KHOSHNOOD, Auteur ; Timothy JIANG, Auteur ; Lina NGUYEN, Auteur ; Lorena MENDEZ, Auteur ; Noemi A. SPINAZZI, Auteur ; Melanie A. MANNING, Auteur ; Michael S. RAFII, Auteur ; Jonathan D. SANTORO, Auteur Langues : Anglais (eng) Mots-clés : Humans Autism Spectrum Disorder/complications/epidemiology/diagnosis Down Syndrome/complications Retrospective Studies Vitamin D Vitamin D Deficiency/complications/epidemiology Autoimmune Diseases/complications Autism spectrum disorder Autoimmune Down syndrome Immunity Neurodevelopmental Trisomy 21 Vitamin D 25-OH Index. décimale : PER Périodiques Résumé : BACKGROUND: Plasma levels of vitamin D have been reported to be low in persons with Down syndrome (DS) and existing data is limited to small and homogenous cohorts. This is of particular importance in persons with DS given the high rates of autoimmune disease in this population and the known relationship between vitamin D and immune function. This study sought to investigate vitamin D status in a multi-center cohort of individuals with DS and compare them to individuals with autism spectrum disorder (ASD) and neurotypical (NT) controls. METHODS: A retrospective, multi-center review was performed. The three sites were located at latitudes of 42.361145, 37.44466, and 34.05349. Patients were identified by the International Classification of Diseases (ICD)-9 or ICD-10 codes for DS, ASD, or well-child check visits for NT individuals. The first vitamin D 25-OH level recorded in the electronic medical record (EMR) was used in this study as it was felt to be the most reflective of a natural and non-supplemented state. Vitamin D 25-OH levels below 30 ng/mL were considered deficient. RESULTS: In total, 1624 individuals with DS, 5208 with ASD, and 30,775 NT controls were identified. Individuals with DS had the lowest mean level of vitamin D 25-OH at 20.67 ng/mL, compared to those with ASD (23.48 ng/mL) and NT controls (29.20 ng/mL) (p < 0.001, 95% CI: -8.97 to -6.44). A total of 399 (24.6%) individuals with DS were considered vitamin D deficient compared to 1472 (28.3%) with ASD and 12,397 (40.3%) NT controls (p < 0.001, 95% CI: -5.43 to -2.36). Individuals with DS with higher body mass index (BMI) were found to be more likely to have lower levels of vitamin D (p < 0.001, 95% CI: -0.3849 to -0.1509). Additionally, having both DS and a neurologic diagnosis increased the likelihood of having lower vitamin D levels (p < 0.001, 95% CI: -5.02 to -1.28). Individuals with DS and autoimmune disease were much more likely to have lower vitamin D levels (p < 0.001, 95% CI: -6.22 to -1.55). Similarly, a history of autoimmunity in a first-degree relative also increased the likelihood of having lower levels of vitamin D in persons with DS (p = 0.01, 95% CI: -2.45 to -0.63). CONCLUSIONS: Individuals with DS were noted to have hypovitaminosis D in comparison to individuals with ASD and NT controls. Associations between vitamin D deficiency and high BMI, personal autoimmunity, and familial autoimmunity were present in individuals with DS. En ligne : https://dx.doi.org/10.1186/s11689-023-09503-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575
in Journal of Neurodevelopmental Disorders > 15 (2023)[article] Hypovitaminosis D in persons with Down syndrome and autism spectrum disorder [texte imprimé] / Natalie K. BOYD, Auteur ; Julia NGUYEN, Auteur ; Mellad M. KHOSHNOOD, Auteur ; Timothy JIANG, Auteur ; Lina NGUYEN, Auteur ; Lorena MENDEZ, Auteur ; Noemi A. SPINAZZI, Auteur ; Melanie A. MANNING, Auteur ; Michael S. RAFII, Auteur ; Jonathan D. SANTORO, Auteur.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 15 (2023)
Mots-clés : Humans Autism Spectrum Disorder/complications/epidemiology/diagnosis Down Syndrome/complications Retrospective Studies Vitamin D Vitamin D Deficiency/complications/epidemiology Autoimmune Diseases/complications Autism spectrum disorder Autoimmune Down syndrome Immunity Neurodevelopmental Trisomy 21 Vitamin D 25-OH Index. décimale : PER Périodiques Résumé : BACKGROUND: Plasma levels of vitamin D have been reported to be low in persons with Down syndrome (DS) and existing data is limited to small and homogenous cohorts. This is of particular importance in persons with DS given the high rates of autoimmune disease in this population and the known relationship between vitamin D and immune function. This study sought to investigate vitamin D status in a multi-center cohort of individuals with DS and compare them to individuals with autism spectrum disorder (ASD) and neurotypical (NT) controls. METHODS: A retrospective, multi-center review was performed. The three sites were located at latitudes of 42.361145, 37.44466, and 34.05349. Patients were identified by the International Classification of Diseases (ICD)-9 or ICD-10 codes for DS, ASD, or well-child check visits for NT individuals. The first vitamin D 25-OH level recorded in the electronic medical record (EMR) was used in this study as it was felt to be the most reflective of a natural and non-supplemented state. Vitamin D 25-OH levels below 30 ng/mL were considered deficient. RESULTS: In total, 1624 individuals with DS, 5208 with ASD, and 30,775 NT controls were identified. Individuals with DS had the lowest mean level of vitamin D 25-OH at 20.67 ng/mL, compared to those with ASD (23.48 ng/mL) and NT controls (29.20 ng/mL) (p < 0.001, 95% CI: -8.97 to -6.44). A total of 399 (24.6%) individuals with DS were considered vitamin D deficient compared to 1472 (28.3%) with ASD and 12,397 (40.3%) NT controls (p < 0.001, 95% CI: -5.43 to -2.36). Individuals with DS with higher body mass index (BMI) were found to be more likely to have lower levels of vitamin D (p < 0.001, 95% CI: -0.3849 to -0.1509). Additionally, having both DS and a neurologic diagnosis increased the likelihood of having lower vitamin D levels (p < 0.001, 95% CI: -5.02 to -1.28). Individuals with DS and autoimmune disease were much more likely to have lower vitamin D levels (p < 0.001, 95% CI: -6.22 to -1.55). Similarly, a history of autoimmunity in a first-degree relative also increased the likelihood of having lower levels of vitamin D in persons with DS (p = 0.01, 95% CI: -2.45 to -0.63). CONCLUSIONS: Individuals with DS were noted to have hypovitaminosis D in comparison to individuals with ASD and NT controls. Associations between vitamin D deficiency and high BMI, personal autoimmunity, and familial autoimmunity were present in individuals with DS. En ligne : https://dx.doi.org/10.1186/s11689-023-09503-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575 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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PermalinkMaternal immune response and air pollution exposure during pregnancy: insights from the Early Markers for Autism (EMA) study / Heather E. VOLK in Journal of Neurodevelopmental Disorders, 12 (2020)
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PermalinkA pilot study of high-dose intravenous immunoglobulin 5% for autism: Impact on autism spectrum and markers of neuroinflammation / Isaac R. MELAMED in Autism Research, 11-3 (March 2018)
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PermalinkRecent progress and considerations for AAV gene therapies targeting the central nervous system / Erik Allen LYKKEN in Journal of Neurodevelopmental Disorders, 10-1 (December 2018)
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