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      Redox Regulation and the Autistic Spectrum: Role of Tryptophan Catabolites, Immuno-inflammation, Autoimmunity and the Amygdala

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          Abstract

          The autistic spectrum disorders (ASD) form a set of multi-faceted disorders with significant genetic, epigenetic and environmental determinants. Oxidative and nitrosative stress (O&NS), immuno-inflammatory pathways, mitochondrial dysfunction and dysregulation of the tryptophan catabolite (TRYCATs) pathway play significant interactive roles in driving the early developmental etiology and course of ASD. O&NS interactions with immuno-inflammatory pathways mediate their effects centrally via the regulation of astrocyte and microglia responses, including regional variations in TRYCATs produced. Here we review the nature of these interactions and propose an early developmental model whereby different ASD genetic susceptibilities interact with environmental and epigenetic processes, resulting in glia biasing the patterning of central interarea interactions. A role for decreased local melatonin and N-acetylserotonin production by immune and glia cells may be a significant treatment target.

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          Maternal infection requiring hospitalization during pregnancy and autism spectrum disorders.

          Hjördis Atladóttir, Poul Thorsen, Lars Domino Østergaard … (2010)
          Exposure to prenatal infection has been suggested to cause deficiencies in fetal neurodevelopment. In this study we included all children born in Denmark from 1980, through 2005. Diagnoses of autism spectrum disorders (ASDs) and maternal infection were obtained through nationwide registers. Data was analyzed using Cox proportional hazards regression. No association was found between any maternal infection and diagnosis of ASDs in the child when looking at the total period of pregnancy: adjusted hazard ratio = 1.14 (CI: 0.96-1.34). However, admission to hospital due to maternal viral infection in the first trimester and maternal bacterial infection in the second trimester were found to be associated with diagnosis of ASDs in the offspring, adjusted hazard ratio = 2.98 (CI: 1.29-7.15) and adjusted hazard ratio = 1.42 (CI: 1.08-1.87), respectively. Our results support prior hypotheses concerning early prenatal viral infection increasing the risk of ASDs.
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            Elevated immune response in the brain of autistic patients.

            Xiaohong Li, Abha Chauhan, Ashfaq M Sheikh … (2009)
            This study determined immune activities in the brain of ASD patients and matched normal subjects by examining cytokines in the brain tissue. Our results showed that proinflammatory cytokines (TNF-alpha, IL-6 and GM-CSF), Th1 cytokine (IFN-gamma) and chemokine (IL-8) were significantly increased in the brains of ASD patients compared with the controls. However the Th2 cytokines (IL-4, IL-5 and IL-10) showed no significant difference. The Th1/Th2 ratio was also significantly increased in ASD patients. ASD patients displayed an increased innate and adaptive immune response through the Th1 pathway, suggesting that localized brain inflammation and autoimmune disorder may be involved in the pathogenesis of ASD.
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              Wild type microglia arrest pathology in a mouse model of Rett syndrome

              Noël C. Derecki, James Cronk, Zhenjie Lu … (2012)
              Rett syndrome is an X-linked autism spectrum disorder. The disease is characterized in the majority of cases by mutation of the MECP2 gene, which encodes a methyl-CpG-binding protein 1–5 . Although MeCP2 is expressed in many tissues, the disease is generally attributed to a primary neuronal dysfunction 6 . However, as shown recently, glia, specifically astrocytes, also contribute to Rett pathophysiology. Here we examined the role of another form of glia, microglia, in a murine model of Rett syndrome. Transplantation of wild type bone marrow into irradiation-conditioned Mecp2-null hosts resulted in engraftment of brain parenchyma by bone marrow-derived myeloid cells of microglial phenotype, and arrest of disease development. However, when cranial irradiation was blocked by lead shield, and microglial engraftment was prevented, disease was not arrested. Similarly, targeted expression of Mecp2 in myeloid cells, driven by Lysmcre on an Mecp2-null background, dramatically attenuated disease symptoms. Thus, via multiple approaches, wild type Mecp2-expressing microglia within the context of an Mecp2-null male mouse arrested numerous facets of disease pathology; lifespan was increased; breathing patterns were normalized; apneas were reduced; body weight was increased to near wild type, and locomotor activity was improved. Mecp2 +/− females also exhibited significant improvements as a result of wild type microglial engraftment. These benefits mediated by wild type microglia, however, were diminished when phagocytic activity was inhibited pharmacologically using annexin V to block phosphatydilserine residues on apoptotic targets, thus preventing recognition and engulfment by tissue-resident phagocytes. These results suggest the importance of microglial phagocytic activity in Rett syndrome. Our data implicate microglia as major players in Rett pathophysiology, and suggest that bone marrow transplantation might offer a feasible therapeutic approach for this devastating disorder.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Neuropharmacol
                Journal ID (iso-abbrev): Curr Neuropharmacol
                Journal ID (publisher-id): CN
                Title: Current Neuropharmacology
                Publisher: Bentham Science Publishers
                ISSN (Print): 1570-159X
                ISSN (Electronic): 1875-6190
                Publication date (Print): March 2014
                Publication date (Electronic): March 2014
                Volume: 12
                Issue: 2
                Pages: 148-167
                Affiliations
                [1 ]CRC, Rm:30, 57 Laurel Street, Glasgow, Scotland
                [ 2 ]Department of Psychiatry, Chulalongkorn University, Bangkok, Thailand
                [3 ]Department of Psychiatry, Deakin University, Geelong, Australia
                Author notes
                [* ]Address correspondence to this author at the George Anderson, CRC, Rm 30, 57 Laurel St. Glasgow G11 7QT, Scotland, UK; Tel: +447 505 623 759; E-mail: anderson.george@ 123456rocketmail.com
                Article
                Publisher ID: CN-12-148
                DOI: 10.2174/1570159X11666131120223757
                PMC ID: 3964746
                PubMed ID: 24669209
                SO-VID: 64a5c1e8-37d3-45da-9ddf-6c769c7dd9ae
                Copyright © ©2014 Bentham Science Publishers
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 18 August 2013
                Date revision received : 18 August 2013
                Date accepted : 2 November 2013
                Categories
                Subject: Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: autism,oxidative stress,nitrosative stress,glia,immuno-inflammation,tryptophan,melatonin.
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: autism, oxidative stress, nitrosative stress, glia, immuno-inflammation, tryptophan, melatonin.

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