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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
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Complement activation in multiple sclerosis plaques: an immunohistochemical analysis.

Gillian Ingram, Sam Loveless, Owain W Howell

  • 1Institute of Infection and Immunity, School of Medicine, Cardiff University, Cardiff, UK. morganbp@cardiff.ac.uk.

Acta Neuropathologica Communications
|June 3, 2014
PubMed
Summary
This summary is machine-generated.

Complement activation is widespread in multiple sclerosis, contributing to nerve damage and disease progression. These findings support targeting complement for multiple sclerosis (MS) monitoring and treatment.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Inflammation and complement activation are implicated in multiple sclerosis (MS) pathology.
  • The precise role in axonal damage, myelin loss, and disease progression requires further clarification.

Purpose of the Study:

  • To investigate the localization and role of complement proteins and regulators in MS lesions.
  • To elucidate the involvement of complement in axonal damage and myelin loss in MS.

Main Methods:

  • Detailed immunohistochemical analysis of brain and spinal cord tissue from MS patients and controls.
  • Examination of active, chronic active, and chronic inactive MS plaques, as well as normal-appearing white matter and cortical areas.

Main Results:

  • Complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, TCC), and regulators (factor H, C1-inhibitor, clusterin) were consistently detected in MS plaques.
  • Complement staining was observed in plaques, peri-plaque areas, normal-appearing white matter, and cortical areas of MS patients, exceeding control levels.
  • Classical pathway activation (C1q staining) was evident in all plaques.
  • Complement components were localized to reactive astrocytes near microglia, myelin, and damaged axons.

Conclusions:

  • Complement is ubiquitously involved in multiple sclerosis.
  • Complement plays a pathogenic role in cell, axon, and myelin damage in MS.
  • Targeting complement pathways presents a potential strategy for MS monitoring and therapy.