Partridge Melissa A, Myers Simon J, Gopinath Sumana, Coorssen Jens R
Department of Molecular Physiology, School of Medicine, University of Western Sydney, Penrith, NSW, Australia.
Molecular Medicine Research Group, School of Medicine, University of Western Sydney, Penrith, NSW, Australia.
Proteomics Clin Appl. 2015 Oct;9(9-10):838-43. doi: 10.1002/prca.201400141. Epub 2015 Apr 11.
Currently in the field of multiple sclerosis (MS) research there is an ongoing debate concerning the cause of the disease. MS is widely considered to begin with an autoimmune dysregulation. The disease does have a prominent autoimmune component however this may be representative of a secondary effect. There is growing evidence that the disease may be initiated by an underlying degeneration of oligodendrocytes. In our viewpoint, we discuss the potential differences between the aetiology and progression of MS. For the most part, proteomic analysis has focused on the autoimmune component of the disease. We suggest that proteomic analysis should be applied to investigating oligodendrocyte degeneration. We discuss the potential of the cuprizone animal model of demyelination and its usefulness in understanding oligodendrocyte degeneration. Immune suppressive therapies are effective at reducing clinical symptoms and improving quality of life. However, a cure is still lacking and as such the disease does still progress. We suggest that if the initiating cause is poorly understood, then curing MS is unlikely.
目前在多发性硬化症（MS）研究领域，关于该疾病的病因存在一场持续的争论。MS被广泛认为始于自身免疫调节异常。该疾病确实有一个显著的自身免疫成分，但这可能是继发效应的表现。越来越多的证据表明，该疾病可能由少突胶质细胞的潜在退化引发。在我们看来，我们讨论了MS病因和进展之间的潜在差异。在很大程度上，蛋白质组学分析聚焦于该疾病的自身免疫成分。我们建议蛋白质组学分析应应用于研究少突胶质细胞退化。我们讨论了脱髓鞘的铜螯合剂动物模型的潜力及其在理解少突胶质细胞退化方面的有用性。免疫抑制疗法在减轻临床症状和改善生活质量方面是有效的。然而，仍然缺乏治愈方法，因此该疾病仍在进展。我们认为，如果引发原因不清楚，那么治愈MS是不太可能的。
