De novo Blood Biomarkers in Autism: Autoantibodies against Neuronal and Glial Proteins.

Loading...
Thumbnail Image

Date

2019-04-29

Journal Title

Journal ISSN

Volume Title

Repository Usage Stats

59
views
22
downloads

Citation Stats

Abstract

Autism spectrum disorders (ASDs) are the most common neurodevelopmental disorders with unidentified etiology. The behavioral manifestations of ASD may be a consequence of genetic and/or environmental pathology in neurodevelopmental processes. In this limited study, we assayed autoantibodies to a panel of vital neuronal and glial proteins in the sera of 40 subjects (10 children with ASD and their mothers along with 10 healthy controls, age-matched children and their mothers). Serum samples were screened using Western Blot analysis to measure immunoglobulin (IgG) reactivity against a panel of 9 neuronal proteins commonly associated with neuronal degeneration: neurofilament triplet proteins (NFP), tubulin, microtubule-associated proteins (tau), microtubule-associated protein-2 (MAP-2), myelin basic protein (MBP), myelin-associated glycoprotein (MAG), α-synuclein (SNCA) and astrocytes proteins such as glial fibrillary acidic protein (GFAP) and S100B protein. Our data show that the levels of circulating IgG class autoantibodies against the nine proteins were significantly elevated in ASD children. Mothers of ASD children exhibited increased levels of autoantibodies against all panel of tested proteins except for S100B and tubulin compared to age-matched healthy control children and their mothers. Control children and their mothers showed low and insignificant levels of autoantibodies to neuronal and glial proteins. These results strongly support the importance of anti-neuronal and glial protein autoantibodies biomarker in screening for ASD children and further confirm the importance of the involvement of the maternal immune system as an index that should be considered in fetal in utero environmental exposures. More studies are needed using larger cohort to verify these results and understand the importance of the presence of such autoantibodies in children with autism and their mothers, both as biomarkers and their role in the mechanism of action of autism and perhaps in its treatment.

Department

Description

Provenance

Citation

Published Version (Please cite this version)

10.3390/bs9050047

Publication Info

Abou-Donia, Mohamed B, Hagir B Suliman, Dario Siniscalco, Nicola Antonucci and Passent ElKafrawy (2019). De novo Blood Biomarkers in Autism: Autoantibodies against Neuronal and Glial Proteins. Behavioral sciences (Basel, Switzerland), 9(5). pp. 47–47. 10.3390/bs9050047 Retrieved from https://hdl.handle.net/10161/20282.

This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.

Scholars@Duke

Suliman

Hagir B. Suliman

Associate Professor in Anesthesiology

Dr. Suliman is an expert in the molecular and cell biology of mammalian diseases, particularly in the molecular regulation of oxidant inflammatory responses in the heart and lung. She has a strong interest and expertise in the transcriptional control of cell metabolism, especially mitochondrial biogenesis and mitochondrial-mediated apoptosis and necrosis. Her recent publications have focused on the redox-regulation of nuclear transcription factors involved in both mitochondrial biogenesis and cellular adaptation to oxidative and nitrosative stress. Specifically, she has undertaken promoter analyses of nuclear respiratory factors-1 and -2 that indicate that these transcription factor genes are controlled by redox-regulated signaling networks activated by reactive oxygen and nitrogen species, and carbon monoxide. Dr. Suliman and her colleagues have reported that the cancer chemotherapeutic, doxorubicin, disrupts cardiac mitochondrial biogenesis through mitochondrial oxidant production, which promotes intrinsic apoptosis, while heme oxygenase-1 up-regulates adaptive mitochondrial biogenesis and opposes apoptosis through close regulation of mitochondrial ROS signaling by physiological CO production, thus forestalling fibrosis and cardiomyopathy. Most recently I have been defining the role of mitochondrial transcription factors in regulating cell survival, proliferation and differentiation including in embryonic stem cells and pluripotent cells.


Unless otherwise indicated, scholarly articles published by Duke faculty members are made available here with a CC-BY-NC (Creative Commons Attribution Non-Commercial) license, as enabled by the Duke Open Access Policy. If you wish to use the materials in ways not already permitted under CC-BY-NC, please consult the copyright owner. Other materials are made available here through the author’s grant of a non-exclusive license to make their work openly accessible.