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Related Experiment Video

Updated: Feb 10, 2026

High-resolution Patterned Biofilm Deposition Using pDawn-Ag43
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Characteristic patterns of complement deposition in NMOSD, MOGAD, and MS.

Yoshiki Takai1,2, Simon Hametner3, Christian Riedl3

  • 1Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan. yoshiki.takai.e6@tohoku.ac.jp.

Acta Neuropathologica
|February 9, 2026
PubMed
Summary
This summary is machine-generated.

Complement system activation differs in CNS inflammatory demyelinating diseases. Neuromyelitis optica spectrum disorders show consistent deposition, while MOGAD and MS exhibit distinct patterns reflecting unique disease paths.

Keywords:
C4dC9neoComplementMOGADMSNMOSD

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Area of Science:

  • Neuroimmunology
  • Pathology

Background:

  • The complement system plays a role in CNS inflammatory demyelinating diseases (IDDs).
  • Its specific involvement in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and multiple sclerosis (MS) remains unclear, unlike in neuromyelitis optica spectrum disorders (NMOSDs).

Purpose of the Study:

  • To histopathologically assess complement system involvement in NMOSD, MOGAD, and MS.
  • To differentiate the roles of complement deposition in the pathogenesis of these IDDs.

Main Methods:

  • Immunohistochemistry was used to examine CNS tissues from patients with NMOSD, MOGAD, and MS.
  • Deposition of complement components C4d, C3d, and C9neo was analyzed in relation to lesion characteristics.

Main Results:

  • NMOSD showed a characteristic perivascular complement deposition pattern in astrocyte-lytic lesions.
  • MOGAD exhibited variable C9neo deposition, distinguishing between types A (preserved oligodendrocytes) and B (oligodendrocyte loss).
  • MS displayed C4d deposits on myelin sheaths in peri-plaque white matter, decreasing with lesion activity.

Conclusions:

  • Distinct complement deposition patterns in NMOSD, MOGAD, and MS suggest different underlying pathogenetic mechanisms.
  • Complement activation is a key feature with specific histopathological correlates in these CNS inflammatory demyelinating diseases.