Division of Geriatric Neurology, Neurology Service, Hospital de Clínicas de Porto Alegre (HCPA), Ramiro Barcelos Street, 2350, Porto Alegre, 90035-903, RS, Brazil.
School of Medicine, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, 90035-903, RS, Brazil.
Neuromolecular Med. 2018 Dec;20(4):491-497. doi: 10.1007/s12017-018-8516-8. Epub 2018 Oct 10.
The purpose of the study was to determine whether Aβ and p-Tau cerebral spinal fluid (CSF) levels can predict progression from amnestic mild cognitive impairment (aMCI) to Alzheimer's disease dementia (ADD) in a 3-year follow-up study. All participants were evaluated blindly by a behavioral neurologist and a neuropsychologist, and classified according to the Petersen criteria for aMCI and according to the Clinical Dementia Rating (CDR) scale. Individuals were also submitted to lumbar puncture at baseline. Levels of Aβ and p-Tau were measured by immunoenzymatic assay. Values were adjusted for age and sex. Thirty-one of 33 (93.9%) participants completed follow-up. Approximately 39% of aMCI individuals progressed to ADD. The relative risk of developing ADD in those with Aβ CSF levels lower than 618.5 pg/mL was 17.4 times higher than in those whose levels were higher than 618.5 pg/mL (P = 0.003). p-Tau alone did not predict progression to ADD (P = 0.101). The relative risk in those with a p-Tau/Aβ ratio higher than 0.135 was 5.7 times greater (P < 0.001). Aβ and p-Tau explained 40.1% of the verbal memory test subscore of the Consortium to Establish a Registry for Alzheimer's Disease (ΔCERADs) variance (P = 0.008). Aβ strongly predicted progression from aMCI to ADD. p-Tau alone, or its relation to Aβ, was inferior than Aβ alone as a predictor of progression to ADD.
这项研究的目的是确定 Aβ 和 p-Tau 脑脊髓液（CSF）水平是否可以预测 3 年随访研究中从遗忘型轻度认知障碍（aMCI）进展为阿尔茨海默病痴呆（ADD）。所有参与者均由行为神经病学家和神经心理学家进行盲法评估，并根据 Petersen 标准诊断为 aMCI，根据临床痴呆评定量表（CDR）进行分类。个体还在基线时接受腰椎穿刺。通过免疫酶联测定法测量 Aβ 和 p-Tau 的水平。根据年龄和性别进行了调整。33 名参与者中有 31 名（93.9%）完成了随访。约 39%的 aMCI 患者进展为 ADD。Aβ CSF 水平低于 618.5 pg/mL 的个体发生 ADD 的相对风险是水平高于 618.5 pg/mL 的个体的 17.4 倍（P = 0.003）。p-Tau 单独不能预测进展为 ADD（P = 0.101）。p-Tau/Aβ 比值高于 0.135 的个体的相对风险高 5.7 倍（P < 0.001）。Aβ 和 p-Tau 解释了 Consortium to Establish a Registry for Alzheimer's Disease（CERADs）语言记忆测试子评分变异的 40.1%（P = 0.008）。Aβ 强烈预测了从 aMCI 到 ADD 的进展。p-Tau 单独或与其与 Aβ 的关系作为进展为 ADD 的预测指标，不如 Aβ 单独。
