ReviewFrontiers in cellular neuroscience2026
Defining functional states and roles of microglia in neuropsychiatric disorders.
Review in Frontiers in cellular neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Neurodevelopmental outcomes relevant to autism in juvenile mice exposed to PCB 11 in the maternal diet throughout gestation and lactation.Frontiers in toxicology · 2026Article
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Authors and funding
3 authors.
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Abstract
Microglia are myeloid cells of the central nervous system (CNS) that acquire a context-specific phenotype and adjust their functions to microenvironmental cues. They participate in immune signaling, synaptic remodeling, and circuit functions, and have emerged as key culprits in neurodevelopmental and psychiatric disorders such as depression, anxiety, autism spectrum disorder (ASD), and schizophrenia. We characterize and discuss different functional state of microglia defined by sc-omics approaches that bring a high resolution to cell functionalities. Subsequently, we review the evidence of microglial states, microglia-driven mechanisms and their impacts on development and progression of neuropsychiatric disorders. In affective mood disorders, chronic stress, glucocorticoid dysregulation, and peripheral inflammation drive microglial nefarious activation. This leads to excessive synaptic pruning, impaired neurotrophic support, glutamate excitotoxicity, and circuit dysfunction in mood-related brain regions, with strong modulation by circadian mechanisms and sex-dependent factors. In ASD, microglia adopt a hybrid activation state characterized by altered inflammatory signaling, dysregulated phagocytosis, and aberrant synaptic pruning, driven by genetic and epigenetic mechanisms, including TREM2, ARID1A, complement components, and calcium-dependent glial signaling, which together disrupt network connectivity and social behavior. In schizophrenia, genetic risk factors related to
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