Grant: Travel Awards - Institute Community Support

The aging process proceeds at different rates across individuals and these variations are not reflected by chronological age (CA)- i.e., the number of years since birth. For example, some people develop age-associated diseases (e.g. cancers, Alzheimer's disease) or noticeable signs of aging (e.g. greying hair) at younger CA than others. There has been interest in finding methods (i.e. biomarkers) that can provide a more detailed assessment of aging. The epigenetic clock has emerged as a key candidate. The clock takes the levels of DNA methylation (DNAm) at some base pairs within the DNA and sums them together resulting in epigenetic age (EA). This is possible because methylation at some DNA regions changes with age. Epigenetic age that is greater than the chronological age of a person (i.e. epigenetic age acceleration) can point to a higher risk of disease or signs of aging. Many different clocks have been built but they do not have consistent accuracy across all adult age groups or sexes. Some tend to be less accurate in older adults (aged 65+) and in females while others show the opposite. These issues lead to misleading association results and need to be addressed in order to make the maximum use of the epigenetic clock in the study of aging. Here, I show that building a new clock by combining multiple previously available ones as well as biological sex can eliminate these shortcomings. I use blood samples from the Canadian Longitudinal Study on Aging (CLSA, n=1445, age range: 45-86 years) to develop the clock and Alzheimer's Disease Neuroimaging Initiative (ADNI, n=1905, age range: 40-96 years) to test its performance.