Autism Spectrum Disorder - Profile, Heterogeneity, Neurobiology and Intervention最新文献

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Associations between Monocyte Cytokine Profiles and Co-Morbid Conditions in Autism Spectrum Disorders 单核细胞因子谱与自闭症谱系障碍共病状况的关系

Autism Spectrum Disorder - Profile, Heterogeneity, Neurobiology and Intervention Pub Date : 2021-01-30 DOI: 10.5772/INTECHOPEN.95548

H. Jyonouchi, L. Geng

{"title":"Associations between Monocyte Cytokine Profiles and Co-Morbid Conditions in Autism Spectrum Disorders","authors":"H. Jyonouchi, L. Geng","doi":"10.5772/INTECHOPEN.95548","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.95548","url":null,"abstract":"Autism spectrum disorder (ASD) is a behaviorally defined syndrome with frequent co-morbidities. Evidence indicate a role of innate immunity in ASD pathogenesis. This study addressed whether innate immune abnormalities are associated with ASD co-morbid conditions and/or other clinical co-variables when assessed as changes in monocyte cytokine profiles. This study included 109 ASD (median 11.5 year) and 26 non-ASD subjects (median 11.4 year). Monocyte cytokine profiles were evaluated in association with age/ethnicity, ASD severity, medications, and co-morbidities present in >15% of ASD subjects [gastrointestinal (GI) symptoms, epilepsy, allergic rhinitis, specific antibody deficiency (SAD), and fluctuating behavioral symptoms resembling pediatric acute-onset neuropsychiatric syndrome (PANS)]. ASD severity did not affect frequency of co-morbid conditions. GI symptoms, epilepsy, SAD, and PANS like symptoms revealed associations with changes in production of tumor necrosis factor-α (TNF-α)/soluble TNF-receptor II (sTNFRII), interleukin-1ß (IL-1ß)/IL-6/IL-10, and IL-6, respectively, mostly independent of other co-variables. ASD severity was associated with changes in multiple cytokines but frequently affected by other clinical co-variables. Our findings revealed associations between specific monocyte cytokine profiles and certain co-morbid conditions in ASD subjects, independent of other clinical co-variables. Our findings will aid in assessing treatment options for ASD co-morbidities and their effects on ASD behavioral symptoms.","PeriodicalId":374742,"journal":{"name":"Autism Spectrum Disorder - Profile, Heterogeneity, Neurobiology and Intervention","volume":"88 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122301327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

L1-79 and the Role of Catecholamines in Autism L1-79和儿茶酚胺在自闭症中的作用

Autism Spectrum Disorder - Profile, Heterogeneity, Neurobiology and Intervention Pub Date : 2020-12-17 DOI: 10.5772/intechopen.95052

J. Rothman

{"title":"L1-79 and the Role of Catecholamines in Autism","authors":"J. Rothman","doi":"10.5772/intechopen.95052","DOIUrl":"https://doi.org/10.5772/intechopen.95052","url":null,"abstract":"A growing body of evidence supports a role for catecholaminergic dysfunction in the core symptoms of autism spectrum disorder (ASD). This paper reviews the direct and indirect role of catecholamines on the central and peripheral nervous systems in ASD. Catecholamines innervate every tissue in the body and almost all tracts of the brain, providing a common neurologic regulatory mechanism for all ASD symptoms. Because the morphology of the catecholaminergic synapse is regulated by growth factors that are released contemporaneously with neurotransmitters, an event that results in abnormally large catecholamine release, will also release high levels of growth factors, which can result in the budding and arborization of nerve terminals. Here, we hypothesize that a hypertrophic synaptic morphology can occur in catecholaminergic systems and increase catecholaminergic tone throughout the body, resulting in an imbalance between catecholaminergic neurologic mechanisms and those that oppose them, and consequently pathology. By exerting a presynaptic effect to inhibit tyrosine hydroxylase and thus the synthesis, storage and release of all catecholamines, L1–79 (a tyrosine hydroxylase inhibitor) may diminish neurotransmitter release and its associated growth factors exerting a therapeutic effect on ASD by reducing the hypertrophic morphology of the synapse and bringing catecholamines back into a homeostatic balance with oppositional neurologic and metabolic influences.","PeriodicalId":374742,"journal":{"name":"Autism Spectrum Disorder - Profile, Heterogeneity, Neurobiology and Intervention","volume":"23 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127075869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1