Schwob N G, Nalbantoglu J, Hastings K E, Mikkelsen T, Cashman N R
Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada.
Ann Neurol. 1990 Jul;28(1):91-4. doi: 10.1002/ana.410280117.
We developed a novel quantitative assay to test the hypothesis that defects in DNA cytosine methylation might be responsible for the brain chromatin abnormalities and transcriptional alterations observed in patients with Alzheimer's disease (AD). We found no significant difference in percent methylation of CCGG sites from brain DNA of 44 patients with AD compared with 20 normal subjects. These results, however, would not exclude genomic redistribution of methylcytosine in AD, or disturbed methylation of a limited population of critical brain-specific genes.
我们开发了一种新型定量检测方法,以检验以下假设:DNA胞嘧啶甲基化缺陷可能是阿尔茨海默病(AD)患者大脑染色质异常和转录改变的原因。我们发现,与20名正常受试者相比,44名AD患者大脑DNA中CCGG位点的甲基化百分比没有显著差异。然而,这些结果并不能排除AD中甲基胞嘧啶的基因组重新分布,或有限数量的关键脑特异性基因的甲基化紊乱。