title: Elevated GFAP Protein in Anterior Cingulate Cortical White Matter in Males With Autism Spectrum Disorder.
abstract: Based on evidence of abnormalities in axon thickness and neuronal disorganization, autism spectrum disorder (ASD) is commonly considered to be a condition resulting from neuronal dysfunction. Yet, recent findings suggest that non-neuronal cell types also contribute to ASD pathology. To investigate the role of glial cells in ASD, a combination of protein and gene expression analyses were used to determine levels of two glial markers, glial fibrillary acidic protein (GFAP) and myelin oligodendrocyte glycoprotein (MOG), in the postmortem brain tissue from control and ASD donors. Levels of GFAP immunoreactivity (ir) were significantly elevated (P = 0.008) in anterior cingulate cortex (Brodmann area 24; BA24) white matter of ASD donors compared to control donors. In contrast, GFAP-ir levels were similar in BA24 gray matter from ASD and control donors. MOG-ir was also similar in both BA24 white and gray matter from ASD and control donors. In anterior prefrontal cortex (BA10), there were no significant differences in GFAP-ir or MOG-ir in either white or gray matter comparing ASD to control donors. Levels of expression of the genes GFAP and MOG also showed no differences between control and ASD donors in BA24 and BA10 white and gray matter. Collectively, these data imply that ASD is associated with an activation of white matter astrocytes in the anterior cingulate cortex as a result of a yet undefined cellular insult. Research is needed to investigate the molecular pathways that underlie this astrocyte reaction and such research may yield important clues regarding the etiology of ASD.
authors.affiliation: Department of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee.
authors.forename: Jessica D
authors.initials: JD
authors.lastname: Crawford
authors.affiliation: Department of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, Tennessee.
authors.forename: Michelle J
authors.initials: MJ
authors.lastname: Chandley
authors.affiliation: Department of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee.
authors.forename: Katalin
authors.initials: K
authors.lastname: Szebeni
authors.affiliation: Department of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee.
authors.forename: Attila
authors.initials: A
authors.lastname: Szebeni
authors.affiliation: Department of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee.
authors.forename: Brandon
authors.initials: B
authors.lastname: Waters
authors.affiliation: Department of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee.
authors.forename: Gregory A
authors.initials: GA
authors.lastname: Ordway
mesh_terms: D000293:Adolescent; D000328:Adult; D000067877:Autism Spectrum Disorder / Q000235:genetics / Q000378:metabolism*; D002648:Child; D002675:Child, Preschool; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism*; D006179:Gyrus Cinguli / Q000378:metabolism*; D006801:Humans; D008297:Male; D066127:White Matter / Q000378:metabolism*; D055815:Young Adult
chemical_list: D005904:Glial Fibrillary Acidic Protein
keywords: cellular neurophysiology; neuroanatomy; neuropathology