Cited by 216Multiple Sclerosis Research StudiesNeuroinflammation and Neurodegeneration MechanismsNeurogenesis and neuroplasticity mechanisms

Oligodendrocytes in the early course of multiple sclerosis

Brück, Wolfgang, Schmied, Mascha, Suchanek, Gerda, Brück, Yvonne, Breitschopf, Helene, Poser, Sigrid, Piddlesden, Sara, Lassmann, Hans·1994·Annals of Neurology

Abstract

The neuropathology of demyelinating lesions in multiple sclerosis was studied in specimens obtained by diagnostic needle biopsy during early stages of the disease. The lesions were characterized by a chronic inflammatory reaction dominated by lymphocytes and macrophages, plaque-like demyelination, and astroglial sclerosis. Oligodendrocytes within the lesions were studied by immunocytochemistry using antibodies against various myelin and oligodendroglia components. The expression of messenger RNA for proteolipid protein was determined by in situ hybridization. Our studies revealed that myelin-oligodendrocyte glycoprotein is a sensitive and reliable marker for identification of oligodendrocytes in demyelinated plaques. The results suggest that in the early course of the disease in some patients, oligodendrocytes may largely be preserved, whereas in others oligodendroglial loss is pronounced. Loss of oligodendrocytes was only marginally related to the stage of demyelinating activity within the lesions. These findings indicate that the pathogenesis of demyelination may vary within different multiple sclerosis patients.

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Crossref · 10.1002/ana.410350111

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  • In cortical grey matter, oligodendrocyte recruitment and remyelination is an early phenomenon in MS lesion formation that occurs in the immediate post-phagocytic phase when foam cells are still abundant in demyelinated lesions.

    “For cortical grey matter, this now indicates that oligodendrocyte recruitment and remyelination is an early phenomenon in MS lesion formation that occurs in the immediate post-phagocytic phase when foam cells are still abundant in the demyelinated lesions.56-60”

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Authors
Brück, W., Schmied, M., Suchanek, G., Brück, Y., Breitschopf, H., Poser, S., Piddlesden, S., & Lassmann, H.
Affiliations
  • University of Göttingen (DE)
  • Austrian Academy of Sciences (AT)
  • Cardiff University (GB)
  • University of Vienna (AT)
Corresponding author
Lassmann, Hans
Venue
Annals of Neurology
Publisher
Wiley
Published
1994-01
Volume
35
Issue
1
Pages
65-73
ISSN
  • 0364-5134 (ISSN-L)
  • 1531-8249
OpenAlex
W2051123512
Cited by
216
References
1
Citations by year
2026: 3 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 2 · 2021: 3 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 4 · 2015: 3 · 2014: 4 · 2013: 4 · 2012: 3
FWCI
12.75
Type
journal article
Language
en
Open access
closed
Locations
  • Annals of Neurology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
oligodendrocytes, multiple sclerosis, demyelination, myelin oligodendrocyte glycoprotein, proteolipid protein, oligodendrocyte loss, demyelinating plaques, chronic inflammation, pathogenesis, early disease course
MeSH terms
Adolescent, Adult, Brain, Female, Humans, Immunohistochemistry, Male, Multiple Sclerosis, Myelin Proteins, Myelin Sheath, Oligodendroglia, Time Factors, In Situ Hybridization

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