Interplay Between VCAM-1 and PGE2 Levels and Autism Spectrum Disorder Severity in Children-A Preliminary...

The clinical heterogeneity of autism spectrum disorders (ASDs) results from dynamic interactions between genetic susceptibility and environmental exposures. Autism is increasingly recognized as involving neuroimmune dysregulation, which may contribute to ASD severity. Several studies indicate that ASD patients exhibit increased levels of VCAM-1, suggesting endothelial dysfunction and enhanced leukocyte infiltration into the brain, which may have adverse bearing on synaptic plasticity, axon growth, and repulsion. Similarly, elevated PGE2 drives microglial activation and excitotoxicity. The present study examines possible links between VCAM-1 and PGE2 levels and ASD severity.

VCAM-1 and PGE₂ concentrations were measured in children with ASD aged 2-6 years and analyzed for age effects and correlations with behavioral severity. Participants were grouped as mild, moderate, or severe based on Autism Diagnostic Observation Schedule-2 (ADOS-2) scores.

VCAM-1 levels were subnormal in 39.3% (n = 24), and PGE₂ levels were above normal in 32.8% (n = 20). Mean VCAM-1 levels decreased significantly with age (F(4, 56) =2.98, p = 0.026) and also, were higher in moderate (U = 36.00, Z = -3.96, p < 0.001) and severe (U = 155.50, Z =-2.70, p = 0.007) ASD groups, with mean ranks rising from 14.46 (mild) to 41.13 (severe). PGE₂ did not differ between severity and age groups (p > 0.05). VCAM-1 correlated moderately with ADOS-2 scores (rho = 0.577, p < 0.001), whereas PGE2 did not (rho = 0.108, p = 0.406), suggesting higher VCAM-1 is linked to increased behavioral severity in ASD.

Inflammation-related biomarkers could be reflecting a heterogeneous set of neuroimmune mechanisms underlying ASD, which may drive behavioral outcomes.