Cellular stress and apoptosis contribute to the pathogenesis of autism spectrum disorder.
Daoyin Dong, Horst Ronald Zielke, David Yeh and 1 others
PMID 29761862WHAT IT FOUND
Post-mortem brain analysis in six autistic males showed elevated cellular stress and cell death markers in the cerebellum, hippocampus, and prefrontal cortex compared to controls.
These findings describe biological mechanisms in deceased patients and do not provide evidence for any clinical intervention.
Key findings
01Markers of endoplasmic reticulum stress were significantly increased in the cerebellum, hippocampus, and prefrontal cortex of autistic brains compared to age-matched controls.
02Proteins indicating apoptosis, specifically cleaved caspase 8 and PARP, were significantly elevated in all three brain regions of autistic subjects.
03Oxidative stress markers, including 4-HNE and nitrotyrosine-modified proteins, were found to be elevated in the autistic brain samples.
STILL TO COME
How it was doneWhat they found
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What it does not show
The sample size was very small, with only six autistic subjects and six controls. All subjects were male, so the findings may not apply to females with autism. The study used post-mortem tissue, meaning the observed biological changes cannot be linked to live clinical symptoms or functional abilities. The study did not identify which specific cell types (neurons or glial cells) were undergoing apoptosis. Differences in the cause of death between groups could potentially influence the results, although the authors argue this is unlikely.
Declared interests
None of the authors declared a conflict of interest.
The easy way to misread this
Do not interpret these cellular findings as evidence that oxidative stress or apoptosis causes autism in living patients, or that treating these pathways will improve symptoms. The study examined post-mortem tissue from only six deceased individuals and describes biological associations rather than proving causation or therapeutic efficacy.