ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020
Complement-Dependent Synaptic Uptake and Cognitive Decline after Stroke and Reperfusion Therapy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.
What it found
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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
55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 citations in OpenAlex.
- Current Advancement and Patient Outcomes in Reperfusion Brain Injuries After Stroke: A Comparative Analysis of Thrombolysis and Thrombectomy.Brain and behavior · 2025Pooled it
- Therapeutic Targeting of the Complement System: From Rare Diseases to Pandemics.Pharmacological reviews · 2021Pooled it
- From Recanalization to Failed Recovery: No Reflow, No Rescue, and No Regrow After Thrombectomy.Translational stroke research · 2026Review
- Dysfunction of hippocampal cells and its role in cognitive impairment.Neural regeneration research · 2026Article
- The ubiquitin E3 ligase TRIM59 in myeloid cell regulates complement C3 through degrading CCAAT/enhancer binding protein β to promote neuron survival after ischemic stroke.Cell & bioscience · 2026Article
- Bindarit attenuates brain injury and neuroinflammation in status epilepticus by disrupting C3/C3aR signaling and modulating microglia-astrocyte interactions.Cell communication and signaling : CCS · 2026Article
- Perivascular SPP1 Drives Microglial Synaptic Engulfment After Ischemic Stroke.CNS neuroscience & therapeutics · 2026Article
- No-reflow phenomenon after vessel recanalization in acute ischemic stroke: mechanisms, diagnosis, and treatment directions.Journal of neurology · 2026Review
- Neurovascular Unit-Derived Extracellular Vesicles as Regulators of Post-Stroke Pathology and Neurorestoration.Biomolecules · 2026Review
- Microglia-neuron communication in ischemic stroke: from homeostatic signaling to pathological remodeling and therapeutic targeting.Frontiers in molecular biosciences · 2026Review
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- Microglia interact with dendritic spines and regulate spine numbers after brain injury following resuscitation from a cardiac arrest.Experimental neurology · 2025Article
- The role of efferocytosis in ischemic stroke and insights from retinopathy.Trends in neurosciences · 2025Review
- Changes in Neuroimmunological Synapses During Cerebral Ischemia.Translational stroke research · 2025Review
- Complement inhibition targets a rich-club within the neuroinflammatory network after stroke to improve radiographic and functional outcomes.Journal of neuroinflammation · 2025Article
- Values of lymphocyte-related ratios in predicting the clinical outcome of acute ischemic stroke patients receiving intravenous thrombolysis based on different etiologies.Frontiers in neurology · 2025Article
- Blood-brain barrier repair: potential and challenges of stem cells and exosomes in stroke treatment.Frontiers in cellular neuroscience · 2025Review
- Repetitive Trans-spinal Magnetic Stimulation Suppresses Microglia to Engulf Synapse and Promotes Nerve Repairment via cGAS-STING Signaling Pathway after Spinal Cord Injury.International journal of biological sciences · 2025Article
- Magnetic targeting enhances the neuroprotective function of human mesenchymal stem cell-derived iron oxide exosomes by delivering miR-1228-5p.Journal of nanobiotechnology · 2024Article
- Mechanisms Underlying Vascular Inflammaging: Current Insights and Potential Treatment Approaches.Aging and disease · 2024Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Despite the success of reperfusion therapy in significantly reducing the extent of infarct expansion after stroke, the effect of revascularization on poststroke neuroinflammation and the role of anti-inflammatory strategies in postreperfusion era are yet to be explored. Here, we investigate whether the neuroinflammatory response may still contribute to neurologic deficits after reperfused stroke by using targeted complement inhibition to suppress poststroke neuroinflammation in mice with or without concurrent reperfusion therapy. Complement inhibition was achieved using B4Crry, an injury site-targeted inhibitor of C3 activation. Following embolic stroke in male C57bl/6 mice, thrombolysis using tissue-plasminogen activator (t-PA) reduced injury and improved motor deficits, but did not improve cognitive outcomes. After both reperfused and non-reperfused stroke, complement activation and opsonization of hippocampal synapses directed ongoing microglia-dependent phagocytosis of synapses for at least 30 d after stroke, leading to a loss of synaptic density that was associated with cognitive decline. B4Crry treatment, alone or in combination with tPA, limited perilesional complement deposition, reduced microgliosis and synaptic uptake, and improved cognitive outcome without affecting regenerative responses. Furthermore, complement inhibition improved the safety, efficacy, and treatment window of reperfusion therapy with t-PA by limiting hemorrhagic transformation. This work thus demonstrates that poststroke neuroinflammation contributes to hemorrhagic transformation and progression of neurodegenerative responses in the brain even following early and successful revascularization.
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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.