This review honors Kurt Jellinger on his 90th birthday as one of the most outstanding neuropathologists, who has contributed immensely to neuroscience due to his vast experience and collection of excellently documented autopsy cases. Two of his many insightful reports are highlighted here. One report focuses on the pathogenesis of inflammatory demyelinating diseases and investigates the neuropathology in autopsy tissue of a patient, who developed an MS-like disease after repeated treatment with lyophilized bovine brain cells in 1958. More than 60 years later, after reinvestigation of the historic samples in 2015 and subsequent mRNA isolation, next generation sequencing and reconstruction of the antibody, we succeeded in identifying myelin oligodendrocyte glycoprotein (MOG) as the target antigen and provided the missing element between the pathomechanisms in classic EAE animal models and transfer of this disease process into humans. A second significant example of Kurt Jellinger’s contribution to neuroscience was a report on the role of MS in the development of Alzheimer's disease (AD), which found that AD pathology is present to the same extent in demyelinated and non-demyelinated cortical areas in MS and the incidence for AD pathology in elderly MS patients is comparable to the normal-aging population. This indicates that chronic inflammation in the MS cortex alone does not significantly predispose to the development of cortical AD pathology. These and other findings were only possible due to the broad collection of extremely well-defined material established by Kurt Jellinger, which ultimately continues to contribute to translational neuroscience, even decades later.

这篇评论向库尔特·杰林格 (Kurt Jellinger) 致敬，在他 90 岁生日之际，他是最杰出的神经病理学家之一，由于他丰富的经验和大量记录在案的尸检病例，他为神经科学做出了巨大贡献。他的许多有见地的报告中有两个在这里突出显示。一份报告侧重于炎症性脱髓鞘疾病的发病机制，并调查了一名患者尸检组织中的神经病理学，该患者在 1958 年用冻干牛脑细胞反复治疗后患上了 MS 样疾病。60 多年后，在重新调查历史悠久的2015 年的样本以及随后的 mRNA 分离、抗体的下一代测序和重建，我们成功地将髓鞘少突胶质细胞糖蛋白 (MOG) 鉴定为靶抗原，并提供了经典 EAE 动物模型中的病理机制与将该疾病过程转移到人类之间的缺失元素。Kurt Jellinger 对神经科学的贡献的第二个重要例子是关于 MS 在阿尔茨海默病 (AD) 发展中的作用的报告，该报告发现 AD 病理学在 MS 的脱髓鞘和非脱髓鞘皮质区域中的存在程度相同，并且老年 MS 患者的 AD 病理学发病率与正常老龄化人群相当。这表明仅 MS 皮质中的慢性炎症不会显着诱发皮质 AD 病理学的发展。