Cytoskeleton proteins in CSF distinguish frontotemporal dementia from AD
Cytoskeleton proteins in CSF distinguish frontotemporal dementia from AD
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DOI：
10.1212/wnl.54.10.1960
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发表时间：
2000-05-23
期刊：
影响因子：
9.9
通讯作者：
Wallin, A
中科院分区：
文献类型：
--
作者：
Sjögren, M;Rosengren, L;Wallin, A
目的和背景：目的探讨额颞叶痴呆（FTD）和其他常见痴呆疾病患者脑脊液中tau蛋白和轻神经丝蛋白（NFL）的水平。两种蛋白质均与FTD的病理生理学有关。研究方法：在18例FTD患者、21例早发性AD（EAD）患者、21例迟发性AD（LAD）患者和18例年龄匹配的对照受试者中研究了CSF tau和NFL水平。结果如下：FTD患者的平均+/- SD CSF NFL水平升高（1442 +/- 1183 pg/mL; p < 0.05）和LAD（1006 +/- 727 pg/mL; p < 0.001）与对照组相比（241 +/- 166 pg/mL），LAD与EAD相比（498 +/- 236 pg/mL; p < 0.05），FTD与EAD相比有升高趋势。与对照受试者（375 +/- 170 pg/mL）相比，EAD（751 +/- 394 pg/mL; p <0.01）和LAD（699 +/- 319 pg/mL; p < 0.01）的CSF tau水平升高，与FTD（354 +/- 140 pg/mL）相比，EAD（p < 0.001）和LAD（p < 0.01）的CSF tau水平升高。CSF NFL与FTD（r = 0.59; p < 0.05）和LAD（r = 0.61; p < 0.01）的认知功能损害程度呈正相关。当比较每个诊断组中具有和不具有APOE-E14等位基因的患者时，未发现CSF NFL或CSF tau的显著差异。结论：结果表明，这些细胞骨架蛋白在FTD和EAD中的差异参与，NFL主要参与FTD的病理生理学，tau参与EAD的病理生理学。在LAD中发现的CSF NFL的增加可能反映了在一定比例的LAD病例中发现的白质变性。
Objective and Background: To investigate the CSF levels of tau and the light neurofilament protein (NFL) in patients with frontotemporal dementia (FTD) and other common dementia disorders as well as normal control subjects. Both proteins have been implicated in the pathophysiology of FTD. Methods: CSF levels of tau and NFL were investigated in 18 patients with FTD, 21 patients with early-onset AD (EAD), 21 patients with late-onset AD (LAD), and 18 age-matched control subjects. Results: Mean +/- SD CSF NFL levels were increased in patients with FTD (1442 +/- 1183 pg/mL; p < 0.05) and LAD (1006 +/- 727 pg/mL; p < 0.001) compared with control subjects (241 +/- 166 pg/mL) and in LAD compared with EAD (498 +/- 236 pg/mL; p < 0.05), and tended to be increased in FTD compared with EAD. CSF tau levels were increased in EAD (751 +/- 394 pg/mL; p < 0.01) and LAD (699 +/- 319 pg/mL; p < 0.01) compared with control subjects (375 +/- 170 pg/mL), and in EAD (p < 0.001) and LAD (p < 0.01) compared with FTD (354 +/- 140 pg/mL). CSF NFL correlated positively with degree of cognitive impairment in FTD (r = 0.59; p < 0.05) and LAD (r = 0.61; p < 0.01). No significant differences were found in CSF NFL or CSF tau when comparing patients who did and did not possess the APOE-epsilon 4 allele within each diagnostic group. Conclusion: The results suggest a differential involvement of these cytoskeleton proteins in FTD and EAD, with NFL primarily involved in the pathophysiology of FTD and tau in that of EAD. The increase in CSF NFL found in LAD might reflect the white-matter degeneration found in a proportion of LAD cases.