Brück W, Schmied M, Suchanek G, Brück Y, Breitschopf H, Poser S, Piddlesden S, Lassmann H
Institute of Neuropathology, University of Göttingen, Germany.
Ann Neurol. 1994 Jan;35(1):65-73. doi: 10.1002/ana.410350111.
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.
在疾病早期通过诊断性穿刺活检获取的标本中,对多发性硬化症脱髓鞘病变的神经病理学进行了研究。这些病变的特征为以淋巴细胞和巨噬细胞为主的慢性炎症反应、斑块状脱髓鞘以及星形胶质细胞硬化。使用针对各种髓鞘和少突胶质细胞成分的抗体,通过免疫细胞化学方法对病变内的少突胶质细胞进行了研究。通过原位杂交确定了蛋白脂蛋白信使核糖核酸的表达。我们的研究表明,髓鞘少突胶质细胞糖蛋白是识别脱髓鞘斑块中少突胶质细胞的敏感且可靠的标志物。结果表明,在疾病早期,一些患者的少突胶质细胞可能在很大程度上得以保留,而在另一些患者中,少突胶质细胞的丢失则很明显。少突胶质细胞的丢失与病变内脱髓鞘活动的阶段仅有微弱关联。这些发现表明,不同多发性硬化症患者的脱髓鞘发病机制可能有所不同。