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    Epigenetic Silencing of Nucleolar rRNA Genes in Alzheimer's Disease

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    Authors
    Pietrzak, Maciej
    Rempala, Grzegorz A.
    Nelson, Peter T.
    Zheng, Jing-Juan
    Hetman, Michal
    Issue Date
    2011-07-22
    URI
    http://hdl.handle.net/10675.2/667
    
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    Abstract
    Background: Ribosomal deficits are documented in mild cognitive impairment (MCI), which often represents an early stage Alzheimer's disease (AD), as well as in advanced AD. The nucleolar rRNA genes (rDNA), transcription of which is critical for ribosomal biogenesis, are regulated by epigenetic silencing including promoter CpG methylation.
    Methodology/Principal Findings: To assess whether CpG methylation of the rDNA promoter was dysregulated across the AD spectrum, we analyzed brain samples from 10 MCI-, 23 AD-, and, 24 age-matched control individuals using bisulfite mapping. The rDNA promoter became hypermethylated in cerebro-cortical samples from MCI and AD groups. In parietal cortex, the rDNA promoter was hypermethylated more in MCI than in advanced AD. The cytosine methylation of total genomic DNA was similar in AD, MCI, and control samples. Consistent with a notion that hypermethylation-mediated silencing of the nucleolar chromatin stabilizes rDNA loci, preventing their senescence-associated loss, genomic rDNA content was elevated in cerebrocortical samples from MCI and AD groups.
    Conclusions/Significance: In conclusion, rDNA hypermethylation could be a new epigenetic marker of AD. Moreover, silencing of nucleolar chromatin may occur during early stages of AD pathology and play a role in AD-related ribosomal deficits and, ultimately, dementia.
    Citation
    PLoS One. 2011 Jul 22; 6(7):e22585
    ae974a485f413a2113503eed53cd6c53
    10.1371/journal.pone.0022585
    Scopus Count
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    Department of Biostatistics and Epidemiology: Faculty Research and Publications

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