多發(fā)性硬化癥（英文：Multiple Sclerosis）是一種慢性,、炎癥性、脫髓鞘的中樞神經(jīng)系統(tǒng)疾病,。多發(fā)性硬化癥的平均發(fā)病年齡一般在20至40歲,，女性發(fā)病人數(shù)兩倍于男性。
多發(fā)性硬化癥的病因不清,，多被認為是自身免疫性疾病,。少數(shù)人認為是一種代謝依賴性神經(jīng)變性疾病。目前尚無有效的治療辦法,。
在多發(fā)性硬化癥（MS）中，腦源性神經(jīng)營養(yǎng)因子（BDNF）提供神經(jīng)保護作用,，但也能通過維護自身反應(yīng)性T細胞促進疾病的發(fā)展,。
但在MS中尚未探索的一個方面就是腦源性神經(jīng)營養(yǎng)因子的前體具有促凋亡作用，兩種蛋白異構(gòu)體,，成熟的腦源性神經(jīng)營養(yǎng)因子BDNF,，這種腦源性神經(jīng)營養(yǎng)因子BDNF促進細胞生存，但截斷型腦源性神經(jīng)營養(yǎng)因子的功能卻是未知的,。
最新研究用Western-blot分析,，發(fā)現(xiàn)血清中成熟型BDNF和腦源性神經(jīng)營養(yǎng)因子前提占總血清中的比例明顯下降，而截斷型腦源性神經(jīng)營養(yǎng)因子卻增加了。
同時研究并沒有發(fā)現(xiàn)腦源性神經(jīng)營養(yǎng)因子異構(gòu)體的比例與臨床或人口特征存在相關(guān)性,。這些結(jié)果表明腦源性神經(jīng)營養(yǎng)因子在多發(fā)性硬化過程中發(fā)揮重要作用,，低水平的腦源性神經(jīng)營養(yǎng)因子前提和高水平的sFas可能通過減少成熟型腦源性神經(jīng)營養(yǎng)因子導(dǎo)致T細胞自身反應(yīng)降低，而截斷型BDNF的增長可能是一種代償機制,。因此,，有關(guān)MS的研究應(yīng)考慮腦源性神經(jīng)營養(yǎng)因子蛋白。（生物谷：Bioon.com）
編譯自：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.
