Arai H, Higuchi S, Sasaki H
Department of Geriatric Medicine, Tohoku University School of Medicine, Sendai, Japan.
Gerontology. 1997;43 Suppl 1:2-10. doi: 10.1159/000213879.
Apolipoprotein E (ApoE) genotyping was conducted in sporadic Alzheimer's disease (AD, n = 91) as well as in other dementing disorders including Parkinson's disease (PD, n = 73), autopsy-confirmed diffuse Lewy body disease (DLBD, n = 16), progressive supranuclear palsy (n = 13), vascular dementia (n = 55), alcoholic dementia (n =25) and normal control subjects (n = 77). ApoE epsilon 4 allele frequency was significantly higher in AD (33.5%, p < 0.001), DLBD (40.6%, p < 0.001) and demented PD (29.4%, p < 0.05) compared to that in normal controls (11.7%). The association of the ApoE epsilon 4 allele with AD was more pronounced in early-onset AD (46.4%) than in late-onset AD (27.8%). 46% of the AD individuals developed AD without association to ApoE epsilon 4, and epsilon 4 homozygotes were found not only in AD, but also in many of other dementing disorders. These results suggest that ApoE genotyping cannot provide certainty about the presence of absence of AD, and that it should be used as an adjunct to other diagnostic tests for AD. On the other hand, cerebrospinal fluid (CSF) tau levels were significantly elevated (p < 0.0001) in AD (78.0 +/- 44.2 pg/ml) compared to those in normal controls (10.6 +/- 8.6 pg/ml). The specificity and the sensitivity of distinguishing AD from normal controls was 95.0 and 91.2%, respectively. Elevated CSF-tau levels were also detected in some patients with acute neurological diseases including meningoencephalitis, Creutzfeld-Jacob disease, normal pressure hydrocephalus and vitamin B12 deficiency encephalopathy. Increased CSF-tau levels in AD were found regardless of the age at onset, clinical stage, ApoE genotype, alpha 1-antichymotrypsin genotype, and presenilin-1 genotype. The CSF-tau levels continued to be abnormal during the progression of AD. These results suggest that CSF-tau serves as an unequivocal and reliable biological marker to aid in the clinical diagnosis of AD.
对散发性阿尔茨海默病(AD,n = 91)以及其他痴呆症进行了载脂蛋白E(ApoE)基因分型,这些痴呆症包括帕金森病(PD,n = 73)、尸检确诊的弥漫性路易体病(DLBD,n = 16)、进行性核上性麻痹(n = 13)、血管性痴呆(n = 55)、酒精性痴呆(n = 25)以及正常对照者(n = 77)。与正常对照者(11.7%)相比,AD(33.5%,p < 0.001)、DLBD(40.6%,p < 0.001)和痴呆型PD(29.4%,p < 0.05)中ApoE ε4等位基因频率显著更高。ApoE ε4等位基因与AD的关联在早发型AD(46.4%)中比在晚发型AD(27.8%)中更明显。46%的AD个体患AD与ApoE ε4无关,并且不仅在AD中发现了ε4纯合子,在许多其他痴呆症中也发现了。这些结果表明,ApoE基因分型不能确定AD的存在与否,它应作为AD其他诊断测试的辅助手段。另一方面,与正常对照者(10.6 ± 8.6 pg/ml)相比,AD患者脑脊液(CSF)中tau水平显著升高(p < 0.0001)(78.0 ± 44.2 pg/ml)。区分AD与正常对照者的特异性和敏感性分别为95.0%和91.2%。在一些患有急性神经系统疾病的患者中也检测到CSF - tau水平升高,这些疾病包括脑膜脑炎、克雅氏病、正常压力脑积水和维生素B12缺乏性脑病。无论发病年龄、临床分期、ApoE基因型、α1 - 抗糜蛋白酶基因型和早老素 - 1基因型如何,AD患者CSF - tau水平均升高。在AD进展过程中,CSF - tau水平持续异常。这些结果表明,CSF - tau是有助于AD临床诊断的明确且可靠的生物学标志物。