英国伦敦大学学院（UCL）的一项研究显示，核磁共振成像扫描与脑脊髓液检测两种手段结合使用，可更有效地对早期阿尔茨海默氏症进行诊断。这意味着将来医生可能在患者没有病症征兆前即可预警阿尔茨海默氏症，并及时进行相应治疗，从而改善该病的治疗效果。

在英国UCL神经病学研究所与阿尔茨海默氏症研究基金的合作研究中，研究人员首先对105名认知能力正常的志愿者的脑脊髓液状况进行了检测，根据脑脊髓液淀粉样蛋白（CSF Aβ1-42）含量的高低，将他们分成两组（其中40人被认定为低水平一组），然后定期对其进行核磁共振成像扫描，以检测他们大脑萎缩的速率。

经过12个月的跟踪检测，研究人员发现，那些脑脊髓液淀粉样蛋白含量低的志愿者，其大脑萎缩的速率比其他人快了一倍；这些人体内APOE4基因（一种可导致阿尔茨海默氏症的风险基因）阳性的几率则比其他人高了近5倍；同时，这些人体内Tao蛋白的含量也较其他人高出许多。Tao蛋白被认为是阿尔茨海默氏症的另一个致病因素。

研究人员指出，三分之一志愿者的脑脊髓液状况与阿尔茨海默氏症病理症状一致，且他们的脑萎缩速率明显增加，这表明，他们可能处于神经退行性病变的最早阶段。而对于阿尔茨海默氏症这种神经退行性疾病来说，早期诊断十分重要。早发现，意味着可在发病初期进行相应的治疗，其治疗效果要好很多。因此，这一发现对于阿尔茨海默氏症的研究具有重要意义。

相关研究结果发表在近期的《神经病学年鉴》上。

推荐原文出处：

Ann Neurol   DOI: 10.1002/ana.22315

Increased brain atrophy rates in cognitively normal older adults with low cerebrospinal fluid Aβ1-42

Jonathan M. Schott MD1,*,?, Jonathan W. Bartlett PhD1,2, Nick C. Fox MD1, Josephine Barnes PhD1, for the Alzheimer's Disease Neuroimaging Initiative Investigators

Abstract

Objective

To identify cognitively normal individuals at risk of Alzheimer disease (AD) based on cerebrospinal fluid (CSF) Aβ1-42, and to determine rates of cerebral atrophy.

Methods

Control subjects from the Alzheimer's Disease Neuroimaging Initiative with CSF and serial magnetic resonance imaging (MRI) were dichotomized on CSF Aβ1-42 (normal control [NC]-high >192pg/ml; NC-low ≤192pg/ml). Baseline and 1-year MRIs were registered, and brain, hippocampal, and ventricular volumes and annualized volume changes were calculated. Baseline characteristics, CSF profiles, neuropsychology, brain volumes and atrophy rates, and APOE, PICALM, CLU, and TOMM40 genotypes were compared. Sample sizes to power presymptomatic clinical trials based on rate of atrophy were calculated.

Results

Forty of 105 (38%) were classified as NC-low, and 65 (62%) as NC-high. There were no differences in age (76.3 ± 5.1 vs 74.9 ± 5.1 years), gender, brain volumes, and all but 1 cognitive score (Trails B; p = 0.015). The NC-low group had higher tau (p = 0.005) and p-tau (p < 0.001), and was more likely to be APOE4 positive (48% vs 11%, p < 0.001). The NC-low group had significantly higher whole brain loss (9.3 vs 4.4ml/yr, p < 0.001), ventricular expansion (2.04 vs 0.95ml/yr, p = 0.002), and hippocampal atrophy rate (0.07 vs 0.03ml/yr, p = 0.029). Baseline Aβ1-42 level was strongly correlated with rate of brain atrophy only in the NC-low group (p < 0.001). Using 141 (95% confidence interval, 86–287) patients per arm provides 80% power in a 1-year treatment trial to show 25% slowing of brain atrophy in the NC-low group.