The 14-3-3 protein in multiple sclerosis: a marker of disease severity
The 14-3-3 protein in multiple sclerosis: a marker of disease severity
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DOI：
10.1191/1352458504ms1089oa
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发表时间：
2004-01-01
影响因子：
5.8
通讯作者：
Mancardi, Gl
中科院分区：
文献类型：
--
作者：
Colucci, M;Roccatagliata, L;Mancardi, Gl
背景：在多发性硬化症（MS）中，轴突损伤是一个早期事件，可能被认为是永久性和进行性残疾的最相关原因。目的：探讨脑脊液14-3-3和tau蛋白的升高作为轴突病理的外周标志物和疾病发展的预测因子的价值。患者和方法：在63例脱髓鞘疾病（DD）患者（包括20例临床分离综合征（CIS）和43例临床定义的MS）以及56例对照者的脑脊液样本中，我们通过免疫印迹分析14-3-3反应性的存在，并通过夹心ELISA分析tau蛋白的浓度。结果：在10个月的平均临床随访中，DD患者14-3-3蛋白CSF反应性阳性的比例（38%）明显高于先前检测到的比例，并且在残疾程度和疾病进展率方面与临床表型更严重的MS患者相关。相反，在DD和对照组中，CSF-tau蛋白的水平变化很大，两组的平均CSF-tau浓度相似。结论：脑脊液14-3-3蛋白的免疫印迹分析可作为识别重度残疾高危DD患者亚组的有效标志物。
Context: In multiple sclerosis ( MS) axonal damage is an early event and is probably to be considered the most relevant cause of permanent and progressive disability. Objectives: To investigate the value of the increase of 14-3-3 and tau proteins in the cerebrospinal fluid (CSF) as peripheral markers of axonal pathology and predictors of disease evolution. Patients and methods: In the CSF samples obtained from 63 patients with demyelinating diseases ( DD), including 20 clinically isolated syndromes (CIS) and 43 clinically defined MS, as well as from 56 controls, we analysed the presence of 14-3-3 reactivity by immunoblot analysis along with the concentration of tau protein by sandwich ELISA. Results: The percentage of DD subjects showing a positive 14-3-3 protein CSF reactivity (38%) was significantly higher than the one previously detected, and was correlated in the MS patients with a more severe clinical phenotype in terms of degree of disability and rate of disease progression, during a 10-month mean clinical follow-up. On the contrary, the levels of the CSF-tau protein were highly variable in DD and control subjects, and the mean CSF-tau concentration was similar in both groups. Conclusions: The immunoblot analysis of 14-3-3 protein in the CSF could be a useful marker to identify a subgroup of DD patients with high risk of developing severe disability.