Congratulations to the Kobor laboratory and collaborators on the publication of their pediatric-focused "epigenetic clock" paper in the prestigious Proceedings of the National Academy of Sciences of the United State of America.
Epigenetic clocks take advantage of the predictable appearance or disappearance methyl groups on DNA (DNA methylation or DNAm) that occur over a person's lifespan to develop algorithms that correlate a particular DNAm state with age. They have been used to infer a person's biological age in relation to their chronological age in order to better understand the process of aging and the onset of various illnesses. People who are biologically older than their chronological age-a process termed "epigenetic age acceleration" tend to have a shorter lifespan and are more prone to diseases such as cancer. We are only beginning to understand how various social and environmental exposures such as chronic stress, socioeconomic status, and diet can influence epigenetic age acceleration.
DNA methylation changes are at their most dynamic during the early childhood years. The Kobor laboratory examined the methylation status on DNA obtained from cheek swabs of children aged just a few months old to late teens in order to develop an epigenetic clock algorithm that specifically takes into account this highly malleable period of development. The resulting clock is highly accurate at predicting chronological age from the methylation status of DNA in healthy individuals.
Armed with this exciting new tool, the Kobor laboratory and their collaborators are now poised to answer several important questions regarding the correlation between epigenetic age and developmental trajectories of children. For example, does epigenetic age acceleration in children (where the epigenetic age is higher than biological age) positively correlate with faster physical and neurological development in children, as opposed to the negative connotations epigenetic age acceleration has in adults? Conversely, does epigenetic age deceleration correlate with slower development? If so, at what point do these epigenetic age deviations switch to having more "adult" connotations?
Read the paper here: The PedBE clock accurately estimates DNA methylation age in pediatric buccal cells