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Complement in Traumatic Brain Injury: Linking Acute Injury to Chronic Neurodegeneration.

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Complement propagates visual system pathology following traumatic brain injury.

Davis M Borucki1,2, Baerbel Rohrer3,4, Stephen Tomlinson5,6

  • 1Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.

Journal of Neuroinflammation
|April 17, 2024
PubMed
Summary
This summary is machine-generated.

Traumatic brain injury (TBI) causes vision loss by activating complement and microglia in the brain. Inhibiting complement preserves synapses and improves vision after TBI.

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Area of Science:

  • Neuroscience
  • Immunology
  • Ophthalmology

Background:

  • Traumatic brain injury (TBI) can lead to delayed and progressive visual system disorders.
  • Neuroinflammation, particularly complement system activation, is implicated in TBI pathogenesis.
  • The role of complement in TBI-induced vision loss remains unexplored.

Purpose of the Study:

  • To investigate the role of complement activation in TBI-induced visual deficits.
  • To examine the effects of complement inhibition on neuroinflammation and synaptic integrity in the dorsal lateral geniculate nucleus (dLGN) and retina after TBI.

Main Methods:

  • A murine model of controlled cortical impact (CCI) was used to induce TBI.
  • Neuroinflammation, histopathology, and visual function were assessed post-TBI.
  • Complement inhibition was achieved using the inhibitor CR2-Crry.

Main Results:

  • TBI induced complement C3 deposition and microglial activation with synaptic internalization in the dLGN.
  • Complement inhibition reduced microglial synaptic uptake and preserved synaptic density.
  • While retinal structure remained unchanged, dLGN neuropathology correlated with reduced visual acuity, which improved with complement inhibition.

Conclusions:

  • TBI triggers complement activation and microglial-mediated synaptic loss in the dLGN, contributing to vision impairment.
  • Complement inhibition mitigates these effects, preserving synaptic integrity and visual function.
  • Targeting the complement system presents a potential therapeutic strategy for TBI-related vision loss.