Dr Alice Kane completed her PhD at the University of Sydney in 2016. She began her postdoctoral training at Dalhousie University in Nova Scotia Canada, exploring the biology of frailty using mouse models. In 2018 she moved to Harvard Medical School in Boston, USA, where she was supported by an NHMRC CJ Martin Biomedical Postdoctoral fellowship, and eventually a National Institutes of Aging K99/R00 award. Here she developed predictive algorithms of age and lifespan based on frailty measures in mice, characterised longitudinal frailty and health in both accelerated and delayed aging mouse models, and developed new approaches for measuring epigenetic markers of aging in mice and humans. She was recruited to be the Ling/Obrzut Assistant Professor at the Institute for Systems Biology, Seattle in 2022 where she led a team exploring sex specific metabolic mechanisms of frailty and female reproductive aging. Dr Kane will be moving to the Charles Perkins Centre at the University of Sydney in 2025.
Research
As humans age they display significant variability in health status and functional ability. Frailty quantitively captures the heterogeneity of aging, and is a measure of biological, rather than chronological age. Those who are frail are at increased risk of falls, hospitalization and mortality. Furthermore, females are more frail than males, yet have a lower mortality risk, and the reasons for this sex-frailty paradox are unknown.
My research aims to identify and disentangle the influence of biological factors (such as hormones and sex chromosomes) and socio-behavioural factors (such as symptom reporting, care-giving) on sex differences in frailty risk and mechanisms. Specifically, we aim to (1) use large human cohort datasets to identify novel social, behavioural, and environmental factors that are differently associated with frailty in females and males; (2) use both mouse and human datasets to identify molecular features (eg. specific blood-based factors, or genetic factors) that are specifically associated with frailty in females or males; and (3) use novel genetically manipulated mouse models to test the separate contributions of sex chromosomes (ie. XX vs XY) and sex hormones (ie. oestrogen or testosterone) on the development of frailty in aging.
This research has the potential to identify novel biomarkers for early frailty detection in men and women, provide a foundation for the identification of sex-specific interventions, and fill critical gaps in sex-specific aging research, ultimately increasing function, quality of life and health for all older Australians.