Epigenetic aging

For the past several years the Ideker lab has had an independent research thread related to using genome-wide methylation profiles to characterize biological aging. These aging studies are somewhat outside of our mainstream research related to cancer molecular networks; however, the field is interesting and growing, with the outcome that our research into epigenetic aging has continued with approximately one interested student in the lab at any given time.

In 2012, in collaboration with the laboratory of Drs. Kang Zhang (UCSD) and Stephen Friend (Sage), we built a quantitative model of aging using measurements at more than 450,000 methylation (CpG) markers from the whole blood of 656 human individuals, aged 19 to 101. This model was able to very accurately predict age from the state of the methylome, which we showed was impacted by gender and genetic variants. We found our aging model was upheld in other human tissues, and that it revealed an advanced aging rate in tumor tissue. 

More recently, we sought to advance the field of epigenetic aging in two ways. First, we partnered with Dr. Howard Fox (formerly TSRI, now University of Nebraska) to explore the effects of viral infection on epigenetic aging rate. In our study, HIV+ men on anti-retroviral therapy had significantly advanced epigenetic aging versus controls [Gross et al. Molecular Cell 2016]. Second, we worked jointly with Dr. Peter Adams (Sanford Burnham Prebys) to study the effects of pro-longevity interventions on epigenetic age in mice. Rapamycin treatment decreased the rate of epigenetic aging, as did caloric restriction and the genetic condition of dwarfism [Wang et al. Genome Biology 2017].