ReviewFrontiers in immunology2026
Neuroinflammatory mechanisms and pharmacological advances in autism spectrum disorder: from inflammatory pathways to targeted interventions.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Autism spectrum disorder (ASD) is highly diverse in causes and symptoms, and reliable biomarkers and mechanism-based treatment targets are still lacking. Neuroinflammation has been linked to ASD risk, symptom development, and long-term course, but the key "body-to-brain" connections and practical intervention points are not yet clearly organized. Methods: We synthesize evidence from clinical immune and cerebrospinal fluid studies, neuroimaging, animal models, and multi-omics research, following a mechanistic path from maternal immune activation (MIA) during pregnancy to postnatal immune imbalance, transmission of inflammatory signals to the brain, and subsequent amplification within the central nervous system. We propose the Peripheral-to-Central Inflammatory Cascade-Amplification Model (PC-ICAM) to summarize actionable nodes and recent pharmacological advances. Results: Within PC-ICAM, ASD-related neuroinflammation follows a cascade from peripheral immune perturbation to peripheral-to-central transmission and central amplification. Peripheral signals may affect the CNS through BBB vulnerability, extracellular vesicle/miRNA communication, and neuro-immune regulatory pathways. Inflammatory signaling involving NF-κB, JAK/STAT, MAPK/ERK, NLRP3, and PI3K-AKT-mTOR may converge with microglial and astrocytic activation, oxidative stress, and mitochondrial dysfunction, disturbing synaptic homeostasis and excitation-inhibition balance. Candidate interventions target IL-6/IL-17 signaling, inflammatory pathways, inflammasome activity, glial modulation, antioxidant/mitochondrial support, BBB stabilization, microbiota-related immune modulation, and exosome-miRNA pathways. Conclusions: PC-ICAM frames ASD-related neuroinflammation as a traceable and actionable peripheral-to-central cascade with amplification, providing a structured map of mechanisms and therapeutic opportunities. It suggests that precision treatment should not rely on a single anti-inflammatory strategy, but rather combine multi-node, mechanism-matched interventions along the cascade.
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