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About the PhD project

Unsuccessful aging is associated with common diseases, such as cardiovascular disease and cancer, which lead to human suffering as well as a heavy socioeconomic burden. In order to understand more about (unsuccessful) aging, scientists are searching for molecular clocks. These clocks chronicle the number of cell divisions (e.g. in cancer) or whether subjects are “biologically” younger or older than their calendar age. Whereas most molecular clocks, such as telomere length, are only poorly associated with age and disease, very promising results were obtained for DNA methylation based (i.e. epigenetic) clocks, such as the Horvath clock. These clocks use genome-wide DNA methylation information as input and rely on basic machine learning techniques to predict (unsuccessful) aging or the number of cell divisions. Whereas these clocks have clearly demonstrated their added value, thus created predictors rely on a large number of loci in the genome, each one with minor impact. It therefore remains unclear to which extent these clocks reflect causal impact or simply track other phenomena such as cell type composition. The aim of the research part of this position is two-fold: (i) to improve our understanding of the mechanism(s) underlying these clocks by evaluating whether clock-associated DNA methylation changes drive gene expression, both quantitatively (amount of gene expression) and qualitatively (splice variants, allelic imbalance), also upon adjustment for cell type composition; (ii) to create better or more convenient clocks for specific case studies, including urine based analyses and cardiovascular disease tracking, also by incorporating insight generated in the first part.

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Prof. dr. ir. Tim De Meyer

tim.demeyer@ugent.be

Vacancy