ReviewFrontiers in neuroscience2026
The relationship between functional brain connectivity and neuroinflammatory processes-new insights into the pathomechanisms of ASD.
Review in Frontiers in neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Research on the role of gut microbiota metabolites in autism by multi-omics and network pharmacology.Frontiers in microbiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by deficits in social communication and restricted, repetitive behaviors. Increasing evidence suggests that neuroinflammatory processes are closely associated with the pathophysiology of ASD, linking immune dysregulation with altered brain development and function. This review synthesizes current findings on the relationships between neuroinflammatory mechanisms, biochemical and metabolic alterations, and functional brain connectivity, as revealed by neuroimaging-particularly functional magnetic resonance imaging (fMRI). Across clinical, postmortem, and imaging studies, individuals with ASD show consistent evidence of microglial and astroglial activation, altered cytokine profiles (including IL-1β, IL-6, and TNF-α), and markers of oxidative stress such as glutathione imbalance and lipid peroxidation. These immune and metabolic alterations are associated with changes in synaptic plasticity, neurotransmission, and large-scale neuronal network organization, including altered functional connectivity within the default mode, salience, and executive control networks. Complementary imaging modalities further support links between glial activity, excitatory-inhibitory imbalance, and aberrant connectivity patterns. Emerging evidence also highlights interactions between inflammation, lipid metabolism, neurotransmitter systems (notably serotonin and dopamine), and genetic and epigenetic factors that modulate immune responses in ASD. Integrating inflammatory and metabolic biomarkers with fMRI and spectroscopic measures provides a promising framework for characterizing biologically informed ASD subtypes and advancing precision diagnostic and therapeutic strategies. Overall, current evidence supports a multilevel neuroimmune framework in which chronic inflammation and oxidative stress are associated with atypical functional brain connectivity in ASD. Future longitudinal and multimodal studies are required to validate candidate biomarkers, clarify mechanistic pathways, and evaluate interventions targeting neuroinflammatory processes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.