Table 1 Commonalities and divergences between ageing and age-related conditions (chronic inflammation, cancer and Alzheimer’s disease)
|  | Chronic inflammation | Cancer | Alzheimer’s disease | |||
|---|---|---|---|---|---|---|
Commonalities with ageinga) | Epigenotype | Genotypic and phenotypic outcome | Epigenotype | Genotypic and phenotypic outcome | Epigenotype | Genotypic and phenotypic outcome |
Chromatin remodelling and di- and tri-methylation of histone H3K4 [82, 87]b) | Increased level of inflammatory cytokines [86] | Common methylation patterns (epigenetic drift) | Redistribution of H4K16ac [110]b) | Changes in the expression of nearby genes | ||
Age-related DNA methylation changes on key genes [142] (e.g. hypomethylation of the tumour necrosis factor (TNF) promoter [88]) | Gene deregulation promoting inflammation | Global DNA hypomethylation and specific promoter hypermethylation In cancer: hyper-methylation of tumour suppressor gene promoters and hypomethylation of repetitive sequences | Silencing of tumour suppressor genes [98] and genome instability [99, 100] | Dysregulation of mechanisms involved in brain development and function | ||
Premature senescence and inflammation | Global methylation level decrease [102], 8-oxo-deoxyguanosine level increase [84] | Low methylation and high 8-oxo-deoxy-guanosine levels are associated with an increased glioma malignancy grade [103] | ||||
Divergences with ageing | Â | Deregulation of epigenetic ageing rate associated with cancer malignancy [96] (e. g. lower epigenetic age in gliomas is associated with poor survival [94]) | - Overall increase of H4K16ac upon ageing and global loss in AD subjects [110] - 27 signatures of AD are age-independent (19 for 5mC, 5 for 5hmC, 3 for 5fC/caC) [111] | |||