The cerebrospinal fluid level of glial fibrillary acidic protein is increased in cerebrospinal fluid from Alzheimer's disease patients and correlates with severity of dementia

被引:65
|
作者
Fukuyama, R [1 ]
Izumoto, T [1 ]
Fushiki, S [1 ]
机构
[1] Kyoto Prefectural Univ Med, Res Inst Neurol Dis & Geriatr, Dept Pathol & Appl Neurobiol, Kamigyo Ku, Kyoto 6028566, Japan
关键词
glial fibrillary acidic protein; cerebrospinal fluid; ELISA; Alzheimer's disease; aging;
D O I
10.1159/000050753
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
To gain insight of the underlying mechanisms of astroglial response to Alzheimer's disease (AD), the level of glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF) from controls and AD subjects were immunochemically determined, and the correlation between that level and dementia severity of AD patients was evaluated. Means and SD of CSF levels of GFAP for the young control group (from 1 to 25 years, mean +/- SD 14.2 +/- 5.0, n = 13) adult control (from 26 to 55 years, 41.6 +/- 10.1, n = 9) and senescent control (older than 56 years, 65.4 +/- 8.0, n = 8) were 2.96 +/- 1.04, 2.80 +/- 1.46 and 3.99 +/- 1.55 ng/ml, respectively, and the CSF level of GFAP was not dependent on age (ANOVA p = 0.17). While that of the AD patient group (n = 27, 70.8 +/- 8.0 years) was 8.96 +/- 7.80 ng/ml, significantly higher than that of both the all-control (3.19 +/- 1.39 ng/ml, t test, p < 0.001) and age-matched senescent (3.99 +/- 1.55 ng/ml, t test, p < 0.005) control groups. The receiver-operator characteristic (ROC) curve revealed that the GFAP concentration at 5 ng/ml in CSF could serve as a cutoff value. The CSF level of GFAP in the moderately to severely demented patients (MMSE <less than or equal to> 17, 13.2 +/- 9.10 ng/ml, n = 9) was approximately by two-fold higher than that of the mildly to moderately demented patients (MMSE greater than or equal to 18, 6.85 +/- 5.76 ng/ml, n = 18; ANOVA, p < 0.05). These findings together with our previous report on an increase in the CSF level of apolipoprotein E suggest that degeneration and stimulation of astrocytes takes place concurrently in the AD brain. Copyright (C) 2001 S.Karger AG, Basel.
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页码:35 / 38
页数:4
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