ArticleExperimental and therapeutic medicine2020
Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Association Between Peripheral IL-6 Levels in the Acute Stage of Stroke and Poststroke Depression: A Systematic Review and Meta-Analysis.Brain and behavior · 2026Pooled it
- Xuming Zhusan Decoction Attenuates Post-Stroke via Modulating TLR4/MYD88/NF-κB Pathway in Mice.Food science & nutrition · 2026Article
- Neutrophil-Related Gene Signatures for Ischemic Stroke Diagnosis.Current medicinal chemistry · 2026Article
- Association of peripheral blood LUBAC and OTULIN expression with severity and outcome in acute ischemic stroke: a prospective cohort study.Frontiers in immunology · 2026Article
- Poststroke anxiety and depression: epidemiology, mechanisms, and management strategies.Frontiers in psychiatry · 2026Review
- Decreased hippocampal neurogenesis and post-stroke depression.Frontiers in psychiatry · 2026Review
- Neurovascular Dysfunction and Glymphatic Impairment: An Unexplored Therapeutic Frontier in Neurodegeneration.International journal of molecular sciences · 2025Review
- Article
- Regulation of L-Lactate in Glutamate Excitotoxicity Under Cerebral Ischemia: Pathophysiology and Preventive Strategy.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Lactylation in post-stroke fatigue: linking metabolic dysregulation to neuroinflammation.Frontiers in neuroscience · 2025Review
- Research Advances in Multimodal Framework-Based Identification and Therapeutic Management of Post-Stroke Depression via the Microbiota-Gut-Brain Axis.Neuropsychiatric disease and treatment · 2025Review
- Cilostazol-inhibited RhoA/NF-κB signaling mitigates hippocampal inflammation and post-stroke depression.Frontiers in pharmacology · 2025Article
- Monoamine signaling and neuroinflammation: mechanistic connections and implications for neuropsychiatric disorders.Frontiers in immunology · 2025Review
- Transcriptomic analysis reveals potential crosstalk genes and immune relationship between triple-negative breast cancer and depression.Discover oncology · 2024Article
- Advancing Post-Stroke Depression Research: Insights from Murine Models and Behavioral Analyses.Life (Basel, Switzerland) · 2024Review
- Pterostilbene improves neurological dysfunction and neuroinflammation after ischaemic stroke via HDAC3/Nrf1-mediated microglial activation.Cellular & molecular biology letters · 2024Article
- Effect of Oxygen-Glucose Deprivation of Microglia-Derived Exosomes on Hippocampal Neurons: A Study on miR-124 and Inflammatory Cytokines.Journal of molecular histology · 2024Article
- Levodopa-Entacapone-Carbidopa Intestinal Gel in the Treatment of Advanced Parkinson's Disease: A Single Center Real-World Experience.Pharmaceutics · 2024Article
- Starting with 24-h levodopa carbidopa intestinal gel at initiation in a large cohort of advanced Parkinson's disease patients.Scientific reports · 2024Article
- Electroacupuncture versus Escitalopram for mild to moderate Post-Stroke Depression: A randomized non-inferiority trial.Frontiers in psychiatry · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence hints to the central role of neuroinflammation in the development of post-stroke depression. Danger signals released in the acute phase of ischemia trigger microglial activation, along with the infiltration of neutrophils and macrophages. The increased secretion of proinflammatory cytokines interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor α (TNFα) provokes neuronal degeneration and apoptosis, whereas IL-6, interferon γ (IFNγ), and TNFα induce aberrant tryptophane degradation with the accumulation of the end-product quinolinic acid in resident glial cells. This promotes glutamate excitotoxicity via hyperexcitation of N-methyl-D-aspartate receptors and antagonizes 5-hydroxy-tryptamine, reducing synaptic plasticity and neuronal survival, thus favoring depression. In the post-stroke period, CX3CL1 and the CD200-CD200R interaction mediates the activation of glial cells, whereas CCL-2 attracts infiltrating macrophages. CD206 positive cells grant the removal of excessive danger signals; the high number of regulatory T cells, IL-4, IL-10, transforming growth factor β (TGFβ), and intracellular signaling via cAMP response element-binding protein (CREB) support the M2 type differentiation. In favorable conditions, these cells may exert efficient clearance, mediate tissue repair, and might be essential players in the downregulation of molecular pathways that promote post-stroke depression.
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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.