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      Neuropsychiatric Disease and Treatment (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on all aspects of neuropsychiatric and neurological disorders. Sign up for email alerts here.

      63,741 Monthly downloads/views I 2.989 Impact Factor I 4.5 CiteScore I 1.09 Source Normalized Impact per Paper (SNIP) I 0.744 Scimago Journal & Country Rank (SJR)

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      Biochemical assessments of thyroid profile, serum 25-hydroxycholecalciferol and cluster of differentiation 5 expression levels among children with autism

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          Abstract

          Background

          The exact pathogenesis of autism is still unknown. Both thyroid hormones and 25(OH)D are important for brain development, in addition to CD5; all have immunomodulatory actions by which their dysregulation may have a potential role in autism pathogenesis.

          Objectives

          The objectives of this study were to assess the thyroid profile, serum 25(OH)D levels and CD5 expression levels among autistic patients and to find out the correlations between the measured biomarkers with each other on one side and with the disease severity on the other side.

          Patients and methods

          This cross-sectional case–control study has been conducted on 60 children with autism and 40 controls, recruited from Qena Governorate, Upper Egypt. Childhood Autism Rating Scale (CARS) score was used to assess the included patients. Biochemical assays of thyroid function in the form of free triiodothyronine (FT3), free tetraiodothyronine (FT4), thyroid-stimulating hormone (TSH) and 25(OH)D were done using commercially available enzyme-linked immunosorbent assay (ELISA) kits, while CD5 expression levels were measured using flow cytometry (FCM) analysis for all the included patients and controls.

          Results

          The overall measurement results show significant higher mean serum TSH levels, mean CD5 expression levels with significant lower mean serum 25(OH)D levels among autistic children when compared with the control group ( p<0.05 for all). Significant negative correlations between CD5 with FT3, FT4 and 25(OH)D were observed. CARS score showed significant negative correlations with both FT3 and 25(OH)D, while it was positively correlated with CD5 in a significant manner ( p<0.05 for all).

          Conclusion

          Elevated CD5 expression and decreased 25(OH)D stores could play a potential role in the pathogenesis of autism via their immune-modulator actions. High TSH serum levels among autistic children, although within the physiological range, reflect the presence of thyroid dysfunction among such children, which needs further assessment.

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          Innate Immunity in multiple sclerosis white matter lesions: expression of natural cytotoxicity triggering receptor 1 (NCR1)

          Pascal Durrenberger, Anna Ettorre, Fatemah Kamel … (2012)
          Background Pathogenic or regulatory effects of natural killer (NK) cells are implicated in many autoimmune diseases, but evidence in multiple sclerosis (MS) and its murine models remains equivocal. In an effort to illuminate this, we have here analysed expression of the prototypic NK cell marker, NCR1 (natural cytotoxicity triggering receptor; NKp46; CD335), an activating receptor expressed by virtually all NK cells and therefore considered a pan-marker for NK cells. The only definitive ligand of NCR1 is influenza haemagglutinin, though there are believed to be others. In this study, we investigated whether there were differences in NCR1+ cells in the peripheral blood of MS patients and whether NCR1+ cells are present in white matter lesions. Results We first investigated the expression of NCR1 on peripheral blood mononuclear cells and found no significant difference between healthy controls and MS patients. We then investigated mRNA levels in central nervous system (CNS) tissue from MS patients: NCR1 transcripts were increased more than 5 times in active disease lesions. However when we performed immunohistochemical staining of this tissue, few NCR1+ NK cells were identified. Rather, the major part of NCR1 expression was localised to astrocytes, and was considerably more pronounced in MS patients than controls. In order to further validate de novo expression of NCR1 in astrocytes, we used an in vitro staining of the human astrocytoma U251 cell line grown to model whether cell stress could be associated with expression of NCR1. We found up-regulation of NCR1 expression in U251 cells at both the mRNA and protein levels. Conclusions The data presented here show very limited expression of NCR1+ NK cells in MS lesions, the majority of NCR1 expression being accounted for by expression on astrocytes. This is compatible with a role of this cell-type and NCR1 ligand/receptor interactions in the innate immune response in the CNS in MS patients. This is the first report of NCR1 expression on astrocytes in MS tissue: it will now be important to unravel the nature of cellular interactions and signalling mediated through innate receptor expression on astrocytes.
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            Brief report: circadian melatonin, thyroid-stimulating hormone, prolactin, and cortisol levels in serum of young adults with autism.

            I. Nir, D Meir, N Zilber … (1995)
            An abnormal circadian pattern of melatonin was found in a group of young adults with an extreme autism syndrome. Although not out of phase, the serum melatonin levels differed from normal in amplitude and mesor. Marginal changes in diurnal rhythms of serum TSH and possibly prolactin were also recorded. Subjects with seizures tended to have an abnormal pattern of melatonin correlated with EEG changes. In others, a parallel was evidenced between thyroid function and impairment in verbal communication. There appears to be a tendency for various types of neuroendocrinological abnormalities in autistics, and melatonin, as well as possibly TSH and perhaps prolactin, could serve as biochemical variables of the biological parameters of the disease.
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              Immune dysfunction and neuroinflammation in autism spectrum disorder.

              Geir Bjorklund, Khaled Saad, Salvatore Chirumbolo … (2016)
              Autism spectrum disorder (ASD) is a complex heterogeneous neurodevelopmental disorder with a complex pathogenesis. Many studies over the last four decades have recognized altered immune responses among individuals diagnosed with ASD. The purpose of this critical and comprehensive review is to examine the hypothesis that immune dysfunction is present more frequently, and it is related to ASD in humans. It was found that that often individuals diagnosed with ASD have alterations in immune cells such as T cells, B cells, monocytes, natural killer cells, and dendritic cells. Also, many individuals diagnosed with ASD have alterations in immunoglobulins and increased autoantibodies. Finally, an important portion of individuals diagnosed with ASD has elevated peripheral cytokines and chemokines and associated neuroinflammation. In conclusion, immune dysregulation and inflammation are important components of ASD diagnosis and are key components of the diagnosis and treatment of ASD.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neuropsychiatr Dis Treat
                Journal ID (iso-abbrev): Neuropsychiatr Dis Treat
                Journal ID (publisher-id): Neuropsychiatric Disease and Treatment
                Title: Neuropsychiatric Disease and Treatment
                Publisher: Dove Medical Press
                ISSN (Print): 1176-6328
                ISSN (Electronic): 1178-2021
                Publication date Collection: 2017
                Publication date (Electronic): 14 September 2017
                Volume: 13
                Pages: 2397-2403
                Affiliations
                [1 ]Department of Neuropsychiatry
                [2 ]Department of Medical Biochemistry and Molecular Biology
                [3 ]Department of Clinical and Chemical Pathology
                [4 ]Department of Pediatrics, Qena Faculty of Medicine, Qena University Hospitals, South Valley University, Qena, Egypt
                Author notes
                Correspondence: Mohammed H Hassan, Department of Medical Biochemistry and Molecular Biology, Qena Faculty of Medicine, South Valley University, Qena, PO Box 83523, Egypt, Tel +20 10 9847 3605, Email mohammedhosnyhassaan@ 123456yahoo.com
                Article
                Publisher ID: ndt-13-2397
                DOI: 10.2147/NDT.S146152
                PMC ID: 5608227
                SO-VID: eaee8d8c-c685-4ecd-9504-3b0fbcb9869f
                Copyright © © 2017 Desoky et al. This work is published and licensed by Dove Medical Press Limited
                License:

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Categories
                Subject: Original Research

                ScienceOpen disciplines: Neurology
                Keywords: thyroid hormones,25(oh)d,cd5,autism,flow cytometry,elisa
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: thyroid hormones, 25(oh)d, cd5, autism, flow cytometry, elisa

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