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Oligodendrocytes in the early course of multiple sclerosis
Author(s) -
Brück Wolfgang,
Schmied Mascha,
Suchanek Gerda,
Brück Yvonne,
Breitschopf Helene,
Poser Sigrid,
Piddlesden Sara,
Lassmann Hans
Publication year - 1994
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410350111
Subject(s) - multiple sclerosis , oligodendrocyte , neuropathology , myelin , immunocytochemistry , pathology , demyelinating disease , pathogenesis , proteolipid protein 1 , in situ hybridization , biology , myelin basic protein , medicine , immunology , central nervous system , neuroscience , disease , messenger rna , biochemistry , gene
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.