Role of Heparin Sulfate in Neuregulin Signaling during Development and in Disease

轴突缺失是多发性硬化症患者临床缺陷的重要原因。由于多发性硬化症的病因尚不清楚，因此不可能确定导致该病轴突损伤的确切事件顺序。对另一种髓鞘相关疾病Pelizaeus-Merzbacher病(PMD)的研究将提供更好的了解PMD中替代(炎症)疾病的机制，这可能在MS磁共振波谱(MRS)和成像(MRI)中也是重要的，以及各种组织学技术将被用来确定该蛋白的关键结构域，介导其轴突维持功能的关键区域，从而试图更好地理解PMD的发病机制和时间进展。希望这些发现将为PMD和MS的临床恶化提供一个模型，并可能导致新的治疗方法。

Axonal loss is an important cause of clinical deficits in patients with MS. Because the etiology of MS is not known, it is impossible to be certain of the precise sequence of events that leads to axonal injury in the disease. The study of another myelin related disorder Pelizaeus- Merzbacher disease (PMD), a disease with a known cause, i.e. mutations affecting the major CNS myelin protein proteolipid protein (PLP1) may provide a better understanding of alternative (to inflammation) disease mechanisms in PMD, which may also be important in MS. Magnetic resonance spectroscopy (MRS), and imaging (MRI), as well as various histological techniques will be utilized to identify the critical domains of this protein that mediate its axon maintaining function in an attempt to better understand the pathogenesis and temporal progression of PMD. Hopefully these findings will provide a model for the clinical deterioration found in PMD as well as MS, and perhaps lead to new therapeutic approaches.