ReviewFrontiers in immunology2025
Bidirectional crosstalk between microglia and serotonin signaling in neuroinflammation and CNS disorders.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- Review
- Metabolic shifts driven by host-microbial interactions.The FEBS journal · 2026Review
- Repurposing Selective Serotonin Reuptake Inhibitors as Immunomodulators: Effects on Macrophage Activation and Polarization.Molecular neurobiology · 2026Review
- Effects of Kongsheng Zhenzhong Pills on Neuroinflammation and cGAS-STING Pathway Activity in BV-2 Microglia.Biomedicines · 2026Article
- A Vortioxetine-Glycyrrhizic Acid Supramolecular Complex: Synthesis and Cellular Effects on Microglial and Blood Cells Under Inflammatory and Glucocorticoid Challenge.Biomedicines · 2026Article
- Glial Cells in Behavioral and Psychological Symptoms of Alzheimer's Disease.International journal of molecular sciences · 2026Review
- The Role of Serotonin in Brain Development: From Molecular Pathways to Neurodevelopmental Risk.Cellular and molecular neurobiology · 2026Review
- Article
- Multi-Omics Reveals Dysregulated Neurotransmitter Systems in Aging and CNS Disorders.Aging cell · 2026Article
- Review
- Tryptophan metabolism alterations in neurological and psychiatric diseases: Molecular mechanisms and pharmacological targets.Metabolic brain disease · 2026Review
- Lower Plasma Serotonin is Associated with Higher Amyloid Burden, Hippocampal Atrophy, and Cognitive decline in Alzheimer's Disease: A 24-Month Longitudinal Study.Journal of molecular neuroscience : MN · 2026Article
- Systems-level investigation of the anxiolytic gut-brain interactions induced by paraprobioticFrontiers in microbiology · 2026Article
- The microbiota-tryptophan-brain axis in neurodegenerative diseases: pathogenic mechanisms, disease-specific roles, and translational therapeutics.Frontiers in microbiology · 2026Review
- Partners in plasticity: serotonergic glial interactions in brain circuit remodeling.Frontiers in neuroscience · 2026Review
- GPCR systems coordinate cellular resilience against aging-associated stress.Frontiers in molecular biosciences · 2026Review
- Article
- A holistic view on disease-modifying aspects, comorbidities, and contemporary neuroprotective approaches.Neuroprotection (Chichester, England) · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammatory processes are increasingly recognized as central to the pathophysiology of diverse central nervous system (CNS) disorders, including major depressive disorder (MDD), Alzheimer's disease (AD), and Parkinson's disease (PD). Microglia, the resident immune effector cells of the CNS, are key regulators of neuroimmune responses and engage in bidirectional communication with the serotonergic system. Activation of microglia toward a pro-inflammatory phenotype can disrupt serotonergic neurotransmission by altering the expression and function of the serotonin transporter (SERT) and modulating downstream 5-HT receptor signaling pathways. Conversely, serotonergic neurotransmission-mediated through receptor subtypes such as 5-HT
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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 Socratic graph.