Journal
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
Volume 76, Issue 1, Pages 27-31Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/jnen/nlw099
Keywords
Alzheimer disease; Cytokines; DNA methylation; Epigenetics; Neuroinflammation; Non-CpG methylation
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Funding
- European Commission [278486]
- Ministerio de Ciencia e Innovacion, Instituto de Salud Carlos III - Fondos FEDER, a Way to Build Europe FIS grant [PI14/00757]
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By means of functional genomics analysis, we recently described the mRNA expression profiles of various genes involved in the neuroinflammatory response in the brains of subjects with late-onset Alzheimer Disease (LOAD). Some of these genes, namely interleukin (IL)-1 beta and IL-6, showed distinct expression profiles with peak expression during the first stages of the disease and control-like levels at later stages. IL-1 beta and IL-6 genes are modulated by DNA methylation in different chronic and degenerative diseases; it is also well known that LOAD may have an epigenetic basis. Indeed, we and others have previously reported gene-specific DNA methylation alterations in LOAD and in related animal models. Based on these data, we studied the DNA methylation profiles, at single cytosine resolution, of IL-1 beta and IL-6 5'-flanking region by bisulphite modification in the cortex of healthy controls and LOAD patients at 2 different disease stages: Braak I-II/A and Braak V-VI/C. Our analysis provides evidence that neuroinflammation in LOAD is associated with (and possibly mediated by) epigenetic modifications.
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