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首页> 外文期刊>Molecular Neurobiology >Characterization of Cerebellum-Specific Ribosomal DNA Epigenetic Modifications in Alzheimer's Disease: Should the Cerebellum Serve as a Control Tissue After All?
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Characterization of Cerebellum-Specific Ribosomal DNA Epigenetic Modifications in Alzheimer's Disease: Should the Cerebellum Serve as a Control Tissue After All?

机译：在阿尔茨海默病患中表征小脑特异性核糖体DNA表观遗传修饰：如果小脑毕竟应该用作对照组织吗？

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摘要

Alzheimer's disease (AD) is a neurodegenerative disease, known as the most common form of dementia. In AD onset, abnormal rRNA expression has been reported to be linked in pathogenesis. Although region-specific expression patterns have previously been reported in AD, it is not until recently that the cerebellum has come under the spotlight. Specifically, it is unclear whether DNA methylation is the mechanism involved in rRNA expression regulation in AD. Hence, we sought to explore the rDNA methylation pattern of two different brain regions - auditory cortex and cerebellum - from AD and age-/sex-matched controls. Our results showed differential hypermethylation at an upstream CpG region to the rDNA promoter when comparing cerebellum controls to auditory cortex controls. This suggests a possible regulatory region from rDNA expression regulation. Moreover, when comparing between AD and control cerebellum samples, we observed hypermethylation of the rDNA promoter region as well as an increase in rDNA content. In addition, we also observed increased rRNA levels in AD compared to control cerebellum. Although still considered a pathology-free brain region, there are growing findings that continue to suggest otherwise. Indeed, cerebellum from AD has been recently described as affected by the disease, presenting a unique pattern of molecular alterations. Given that we observed that increased rDNA promoter methylation did not silence rDNA gene expression, we suggest that rDNA promoter hypermethylation is playing a protective role in rDNA genomic stability and, therefore, increasing rRNA levels in AD cerebellum.
机译：阿尔茨海默病（AD）是一种神经变性疾病，称为最常见的痴呆形式。在AD发作中，据报道，据报道了异常的RRNA表达在发病机制中联系在一起。尽管在AD中先前已经报告了地区特异性表达模式，但直到最近，小脑都在聚光灯下来。具体而言，目前尚不清楚DNA甲基化是否是AD中rRNA表达调节的机制。因此，我们试图探索两种不同脑区的甲基化模式 - 来自广告和年龄/性别匹配的对照组。当比较小脑对照对听觉皮质控制时，我们的结果在上游CPG区域显示到RDNA启动子的差异高甲基化。这表明来自RDNA表达调节的可能调节区。此外，当AD和对照细胞样品之间比较时，我们观察到RDNA启动子区的高甲基化以及RDNA含量的增加。此外，与对照细胞相比，我们还观察到AD中的RRNA水平增加。虽然仍然被认为是一种无病理脑区，但是正在越来越多地建议另有说明。实际上，来自广告的小脑已被描述为受疾病的影响，呈现出独特的分子改变模式。鉴于我们观察到增加的RDNA启动子甲基化没有沉默RDNA基因表达，我们建议RDNA启动子高甲基化在RDNA基因组稳定性中发挥保护作用，因此增加了AD小脑中的RRNA水平。

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