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Table 1 Commonalities and divergences between ageing and age-related conditions (chronic inflammation, cancer and Alzheimer’s disease)

From: Wandering along the epigenetic timeline

  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) Cell vulnerable to mutations [96, 97] 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] Accumulation of 5hmC, 5fC and 5caC [111, 113, 114] Dysregulation of mechanisms involved in brain development and function
Overexpression of histone acetyl-transferase P300 [83, 89] 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   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]
  1. aIn the disease the common trait is exaggerated
  2. bH3K4 = lysine 4 on histone 3, H4K16ac = acetylation of lysine 16 on histone 4
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