Objective:

To synthesize evidence on neuroinflammation's role in Autism Spectrum Disorder (ASD) and propose targeted therapeutic interventions that could improve clinical outcomes.

Key Findings:

• Neuroinflammation in ASD follows a cascade from peripheral immune perturbation to central nervous system amplification.
• Key inflammatory pathways include NF-κB, JAK/STAT, MAPK/ERK, and others that disrupt synaptic homeostasis.
• Candidate interventions target various inflammatory pathways, such as IL-6/IL-17 signaling and glial modulation, aiming to restore immune balance and neural function.

Interpretation:

The PC-ICAM framework provides a structured understanding of neuroinflammation in ASD, highlighting the need for multi-targeted therapeutic strategies rather than single anti-inflammatory approaches, and suggesting directions for future research.

Limitations:

• Current understanding of neuroinflammation's dynamic features across developmental stages is incomplete, necessitating urgent research efforts.
• The molecular networks linking inflammation to neural dysfunction require further investigation to clarify their roles.

Conclusion:

A comprehensive approach to ASD treatment should integrate multiple mechanism-based interventions targeting neuroinflammation to improve outcomes.