Elevated GFAP Protein in Anterior Cingulate Cortical White Matter in Males With Autism Spectrum Disorder.
Autism brains show overactive astrocytes in white matter, adding a new layer to why connectivity falters.
01Research in Context
What this study did
Scientists looked at brain tissue from adults with autism after death. They measured GFAP, a protein that shows when support cells called astrocytes are active. They focused on white matter in the anterior cingulate, a spot that helps control attention and emotions.
The team compared the autism group to donors without autism. They also checked two other brain chemicals to see if they changed too.
What they found
GFAP levels were higher in the autism group. The boost was in the white matter of the anterior cingulate. The other chemicals stayed the same.
This means astrocytes in that area were more active, not dead or missing.
How this fits with other research
Storch et al. (2012) saw more microglia, a different support cell, in the same kind of brain samples. Both studies point to glial cells acting up in autism, but in different cell types.
Fitzgerald et al. (2019) used brain scans and found weak white-matter wires across the whole brain in living people with autism. Spriggs et al. (2015) now show one reason why: the support cells in that wire coating are on high alert.
Capio et al. (2013) watched kids with autism and saw their white-matter maturation stall. The new study adds that by adulthood, the stalled wires also carry signs of chronic astrocyte stress.
Why it matters
You cannot test GFAP in a living client, but you can remember that white-matter problems in autism are not just about missing wires. Inflamed support cells may add noise to neural networks. When you see attention or flexibility issues, picture both the wires and the glue around them. This view keeps you open to future medical referrals and reminds you why calm, predictable sessions help brains that are already on high alert.
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02At a glance
03Original 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.
Autism research : official journal of the International Society for Autism Research, 2015 · doi:10.1002/aur.1480