Blood-brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders.
Maria Fiorentino, Anna Sapone, Stefania Senger and 6 others
PMID 27957319WHAT IT FOUND
In postmortem brains and intestinal biopsies from people with autism, researchers found altered blood-brain barrier and gut barrier proteins.
These molecular changes suggest a possible gut-brain axis dysfunction but do not prove it causes autism.
Key findings
01In the cortex of subjects with autism, genes for blood-brain barrier tight junction proteins claudin-3, claudin-5, claudin-12 and tricellulin were upregulated compared to controls.
02Western blot analysis confirmed higher protein levels of claudin-5 in the cortex of subjects with autism, but showed reduced claudin-12 protein, contradicting the gene expression data for that specific protein.
03In duodenal biopsies from patients with autism, 75% showed decreased expression of at least one barrier-forming tight junction component, and 66% showed increased levels of pore-forming claudins.
STILL TO COME
How it was doneWhat they found
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What it does not show
The study is descriptive and cannot prove that these molecular changes cause autism or its symptoms. Sample sizes were very small, which limits the reliability of the findings. Postmortem brain tissue is subject to confounding factors like medication use, cause of death, and tissue preservation time. The control groups for the brain and gut analyses differed; gut controls had gastrointestinal symptoms, while brain controls had no known neurological disorders. There was a discrepancy between gene expression and protein levels for claudin-12, suggesting complex regulatory mechanisms not fully understood.
The easy way to misread this
Do not assume these barrier alterations are the cause of autism or that they are present in all living patients. The study used postmortem tissue and small numbers of living biopsies, so these findings are preliminary molecular observations, not diagnostic markers.