Altered DNA methylation profiles in blood from patients with sporadic Creutzfeldt–Jakob disease

Prion diseases are fatal and transmissible neurodegenerative disorders caused by the misfolding and aggregation of prion protein. Although recent studies have implicated epigenetic variation in common neurodegenerative disorders, no study has yet explored their role in human prion diseases. Here we...

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Bibliographic Details
Published in:Acta neuropathologica 2020-12, Vol.140 (6), p.863-879
Main Authors: Dabin, Luke C., Guntoro, Fernando, Campbell, Tracy, Bélicard, Tony, Smith, Adam R., Smith, Rebecca G., Raybould, Rachel, Schott, Jonathan M., Lunnon, Katie, Sarkies, Peter, Collinge, John, Mead, Simon, Viré, Emmanuelle
Format: Article
Language:English
Subjects:
Alzheimer's disease
Cortex (frontal)
Creutzfeldt-Jakob disease
Data mining
Deoxyribonucleic acid
Disease
DNA
DNA methylation
DNA probes
Epigenetic inheritance
Epigenetics
Ethylenediaminetetraacetic acid
Genetic research
Genomes
Genomics
Learning algorithms
Machine learning
Medical research
Medicine
Medicine & Public Health
Medicine, Experimental
Methylation
Nervous system diseases
Neurodegenerative diseases
Neurosciences
Original Paper
Pathology
Prion protein
Prions
Protein folding
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Summary:Prion diseases are fatal and transmissible neurodegenerative disorders caused by the misfolding and aggregation of prion protein. Although recent studies have implicated epigenetic variation in common neurodegenerative disorders, no study has yet explored their role in human prion diseases. Here we profiled genome-wide blood DNA methylation in the most common human prion disease, sporadic Creutzfeldt–Jakob disease (sCJD). Our case–control study ( n  = 219), when accounting for differences in cell type composition between individuals, identified 38 probes at genome-wide significance ( p  
ISSN:0001-6322
1432-0533
DOI:10.1007/s00401-020-02224-9