The epigenetic clock has increasingly become known as a way of determining biological age based on DNA methylation rather than a particular chronological age. Epigenetics examines how external factors change genes expression, DNA methylation is the process of transferring a methyl group onto the C5 position of the cytosine to form 5-methylcytosine (Moore et al., 2013) (Fig.3), this changes the expression of the gene without altering the genetic code of the organism (Shamsi et al., 2017). Therefore, this change will have an impact on the interaction between e.g. proteins and how the DNA strand is read, suppressing or activating genes (Adamik et al., 2019).
The epigenetic clock can be used to determine health status and potential disease risk such as that of Alzheimer’s or cancer, and even all-cause mortality (S. Sharma et al., 2009). Furthermore, as well as a form of identifying potential health risk, the changes in the epigenome itself suggest that they may play a major role in disease causation (Shamsi et al., 2017). DNA methylation has been observed to directly affect imprinted gene regulation (Zoghbi & Beaudet, 2016)(Smith et al., 2007).
Species-specific epigenetic clocks have been developed based on the combined methylation status of hundreds of CpG sites (regions where a guanine nucleotide comes after a cytosine nucleotide within DNA, in the 5’ -> 3’ direction) leading to debate as to the biological implications of genes associated with the clock and whether the ‘clock’ is in fact a switch promoting biological ageing or disease.
