多发性硬化症（英文：Multiple Sclerosis）是一种慢性、炎症性、脱髓鞘的中枢神经系统疾病。多发性硬化症的平均发病年龄一般在20至40岁，女性发病人数两倍于男性。
多发性硬化症的病因不清，多被认为是自身免疫性疾病。少数人认为是一种代谢依赖性神经变性疾病。目前尚无有效的治疗办法。
在多发性硬化症（MS）中，脑源性神经营养因子（BDNF）提供神经保护作用，但也能通过维护自身反应性T细胞促进疾病的发展。
但在MS中尚未探索的一个方面就是脑源性神经营养因子的前体具有促凋亡作用，两种蛋白异构体，成熟的脑源性神经营养因子BDNF，这种脑源性神经营养因子BDNF促进细胞生存，但截断型脑源性神经营养因子的功能却是未知的。
最新研究用Western-blot分析，发现血清中成熟型BDNF和脑源性神经营养因子前提占总血清中的比例明显下降，而截断型脑源性神经营养因子却增加了。
同时研究并没有发现脑源性神经营养因子异构体的比例与临床或人口特征存在相关性。这些结果表明脑源性神经营养因子在多发性硬化过程中发挥重要作用，低水平的脑源性神经营养因子前提和高水平的sFas可能通过减少成熟型脑源性神经营养因子导致T细胞自身反应降低，而截断型BDNF的增长可能是一种代偿机制。因此，有关MS的研究应考虑脑源性神经营养因子蛋白。（生物谷：Bioon.com）
编译自：Altered serum content of brain-derived neurotrophic factor isoforms in multiple sclerosis
doi:10.1016/j.jns.2012.07.016
PMC:
PMID:
Altered serum content of brain-derived neurotrophic factor isoforms in multiple sclerosis
Enrico Tongiorgia, Arianna Sartorib,et al.
In multiple sclerosis (MS), brain-derived neurotrophic factor (BDNF) provides neuroprotection, but can also promote disease through the maintenance of autoreactive T cells. One aspect that has not been explored yet in MS is related to the opposite functions of BDNF protein isoforms consisting of the pro-BDNF precursor, which has pro-apoptotic effects, and two proteolytic isoforms, the mature BDNF with pro-survival effects and truncated BDNF, with unknown functions. Using ELISA and semi-quantitative Western-blot we determined the relative serum levels of BDNF isoforms in 2 relapsing–remitting MS patients without any disease modifying therapy and 2 age and gender-matched healthy controls and searched for clinical correlates. Total serum BDNF was lower in MS than in HC. We demonstrate that the capture and detection antibodies of the ELISA kit from Promega are able to recognize all three isoforms but with different efficiency. Using Western-blot analysis, we show that the percentage of serum mature BDNF and pro-BDNF with respect to total serum BDNF was significantly decreased, while truncated BDNF was increased. No correlation between BDNF isoform percentage and clinical or demographic features was found. Serum Fas (sFas) was increased. These results support and expand the current hypothesis on the role of BDNF in multiple sclerosis, in that low pro-BDNF and high sFas might result in a failure to limit autoreactive T cells by apoptotic deletion and decreased mature BDNF may not provide enough neuroprotection, while truncated BDNF percent increase could be a compensatory mechanism. Hence, future studies on MS should take into account BDNF proteolytic processing.
