Conserved epigenomic signals in mice and humans reveal immune basis of Alzheimer’s disease

Elizabeta Gjoneska, Andreas R. Pfenning, Hansruedi Mathys, Gerald Quon, Anshul Kundaje, Li-Huei Tsai () and Manolis Kellis ()
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Elizabeta Gjoneska: The Picower Institute for Learning and Memory, Massachusetts Institute of Technology
Andreas R. Pfenning: Broad Institute of Harvard University and Massachusetts Institute of Technology
Hansruedi Mathys: The Picower Institute for Learning and Memory, Massachusetts Institute of Technology
Gerald Quon: Broad Institute of Harvard University and Massachusetts Institute of Technology
Anshul Kundaje: Broad Institute of Harvard University and Massachusetts Institute of Technology
Li-Huei Tsai: The Picower Institute for Learning and Memory, Massachusetts Institute of Technology
Manolis Kellis: Broad Institute of Harvard University and Massachusetts Institute of Technology

Nature, 2015, vol. 518, issue 7539, 365-369

Abstract: Analysis of transcriptional and epigenomic changes in the hippocampus of a mouse model of Alzheimer’s disease shows that immune function genes and regulatory regions are upregulated, whereas genes and regulatory regions involved in synaptic plasticity, learning and memory are downregulated; genetic variants associated with Alzheimer’s disease are only enriched in orthologues of upregulated immune regions, suggesting that dysregulation of immune processes may underlie Alzheimer’s disease predisposition.

Date: 2015
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DOI: 10.1038/nature14252

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