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Related Experiment Videos

Complement activated C4d immunoreactive oligodendrocytes delineate small cortical plaques in multiple sclerosis.

Claudia Schwab1, Patrick L McGeer

  • 1Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, British Columbia V6T 1Z3, Canada.

Experimental Neurology
|March 1, 2002
PubMed
Summary

Complement-activated oligodendrocytes (CAOs) mark early, small lesions in multiple sclerosis (MS). This suggests complement plays a role in initiating MS demyelination, potentially offering a reversible stage.

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Area of Science:

  • Neuroimmunology
  • Neuropathology

Background:

  • Complement-activated oligodendrocytes (C4d-CAOs) are implicated in neurodegeneration but unstudied in multiple sclerosis (MS).
  • Early stages of MS pathology remain incompletely understood.

Purpose of the Study:

  • To investigate the presence and significance of C4d-CAOs in multiple sclerosis lesions.
  • To determine the role of complement activation in the earliest stages of MS plaque formation.

Main Methods:

  • Immunohistochemical analysis of MS brain tissue using antibodies against C4d and other complement components (C1q-C9).
  • Characterization of miniature demyelinated plaques associated with C4d-CAOs, including myelin and axonal integrity assessment.

Main Results:

  • C4d-CAOs were identified, delineating miniature MS plaques (300-500 µm) devoid of myelin and surrounded by activated microglia.

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  • Axons within these miniature plaques appeared undamaged, despite swollen oligodendroglial processes.
  • In contrast, larger MS lesions showed immunoreactivity for the full complement cascade (C1q-C9).

    • Conclusions:

    • Miniature plaques bordered by C4d-CAOs may represent the earliest stage of MS lesion development.
    • The findings suggest a direct attack on oligodendroglia by early complement components as a potential initiating event in MS.
    • Incomplete complement activation in early lesions implies a potentially reversible process, unlike full activation in larger lesions leading to permanent damage.