英國(guó)倫敦大學(xué)學(xué)院（UCL）的一項(xiàng)研究顯示，核磁共振成像掃描與腦脊髓液檢測(cè)兩種手段結(jié)合使用,，可更有效地對(duì)早期阿爾茨海默氏癥進(jìn)行診斷,。這意味著將來(lái)醫(yī)生可能在患者沒有病癥征兆前即可預(yù)警阿爾茨海默氏癥,，并及時(shí)進(jìn)行相應(yīng)治療，從而改善該病的治療效果,。
在英國(guó)UCL神經(jīng)病學(xué)研究所與阿爾茨海默氏癥研究基金的合作研究中,，研究人員首先對(duì)105名認(rèn)知能力正常的志愿者的腦脊髓液狀況進(jìn)行了檢測(cè)，根據(jù)腦脊髓液淀粉樣蛋白（CSF Aβ1-42）含量的高低,，將他們分成兩組（其中40人被認(rèn)定為低水平一組）,，然后定期對(duì)其進(jìn)行核磁共振成像掃描，以檢測(cè)他們大腦萎縮的速率,。
經(jīng)過(guò)12個(gè)月的跟蹤檢測(cè),，研究人員發(fā)現(xiàn)，那些腦脊髓液淀粉樣蛋白含量低的志愿者,，其大腦萎縮的速率比其他人快了一倍,；這些人體內(nèi)APOE4基因（一種可導(dǎo)致阿爾茨海默氏癥的風(fēng)險(xiǎn)基因）陽(yáng)性的幾率則比其他人高了近5倍,；同時(shí)，這些人體內(nèi)Tao蛋白的含量也較其他人高出許多,。Tao蛋白被認(rèn)為是阿爾茨海默氏癥的另一個(gè)致病因素,。
研究人員指出，三分之一志愿者的腦脊髓液狀況與阿爾茨海默氏癥病理癥狀一致,，且他們的腦萎縮速率明顯增加,，這表明，他們可能處于神經(jīng)退行性病變的最早階段,。而對(duì)于阿爾茨海默氏癥這種神經(jīng)退行性疾病來(lái)說(shuō),，早期診斷十分重要。早發(fā)現(xiàn),，意味著可在發(fā)病初期進(jìn)行相應(yīng)的治療,，其治療效果要好很多。因此,，這一發(fā)現(xiàn)對(duì)于阿爾茨海默氏癥的研究具有重要意義,。
相關(guān)研究結(jié)果發(fā)表在近期的《神經(jīng)病學(xué)年鑒》上。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
