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Related Experiment Video

Updated: Dec 24, 2025

Author Spotlight: Establishing a Reliable Distal MCA Occlusion Model in Mice for Stroke Research
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Complement-Dependent Synaptic Uptake and Cognitive Decline after Stroke and Reperfusion Therapy.

Ali M Alawieh1,2, E Farris Langley2, Wuwei Feng3

  • 1Department of Neurosurgery, Emory University School of Medicine, Atlanta, Georgia 30322 tomlinss@musc.edu aalawie@emory.edu.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|April 16, 2020
PubMed
Summary

Targeted complement inhibition reduces neuroinflammation after stroke, improving cognitive function and limiting hemorrhagic transformation. This strategy enhances reperfusion therapy efficacy and safety, even after successful revascularization.

Keywords:
cognitive outcomescomplementreperfusionstroketissue-plasminogen activator

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Reperfusion therapy significantly reduces stroke infarct size but doesn't fully restore cognitive function.
  • Post-stroke neuroinflammation, particularly complement activation, persists and contributes to synaptic loss and cognitive deficits.
  • The role of neuroinflammation in hemorrhagic transformation and treatment efficacy after reperfusion is not well understood.

Purpose of the Study:

  • To investigate the contribution of neuroinflammation to cognitive deficits after reperfused stroke.
  • To evaluate the efficacy of targeted complement inhibition in suppressing post-stroke neuroinflammation.
  • To determine if complement inhibition improves outcomes and safety of reperfusion therapy.

Main Methods:

  • Embolic stroke model in mice with or without tissue-plasminogen activator (t-PA) reperfusion therapy.
  • Administration of B4Crry, an injury site-targeted inhibitor of C3 activation, to suppress complement.
  • Assessment of neuroinflammation, synaptic density, cognitive function, and hemorrhagic transformation.

Main Results:

  • t-PA reduced infarct size and improved motor deficits but not cognitive outcomes.
  • Complement activation and synaptic phagocytosis occurred in both reperfused and non-reperfused strokes, leading to cognitive decline.
  • B4Crry treatment limited complement deposition, microgliosis, and synaptic uptake, improving cognitive outcomes.
  • Complement inhibition improved the safety, efficacy, and treatment window of t-PA by reducing hemorrhagic transformation.

Conclusions:

  • Post-stroke neuroinflammation, driven by complement activation, contributes to cognitive deficits and neurodegeneration even after successful reperfusion.
  • Targeted complement inhibition is a promising strategy to mitigate neuroinflammation, improve cognitive outcomes, and enhance the safety and efficacy of reperfusion therapy.
  • Complement inhibition addresses key challenges in stroke treatment: functional recovery and hemorrhagic transformation.