The molecular sciences research theme works to understand how the experiences you have had in your life shape the way your genes work and, ultimately, the length and quality of your life. We compare markers of your body’s age to your calendar age to understand the natural history of aging and find opportunities to promote wellbeing throughout the lifecourse.

Does the body age independently of the calendar?

Life expectancies have increased substantially over the past century. But are extended lifespans lived in good health?

In Australia and the US, levels of chronic physical and mental disability have increased in our aging populations. Is there a way we could increase human ‘health spans’?

The rate at which we age has direct consequences for our health and mental functioning – and not just for neurodegenerative conditions like Alzheimer’s disease.

Little is known about the developmental origins of aging. What are the risk and protective factors that we might build in childhood, adolescence, and young adulthood? Research doesn’t yet know.

Researchers must better understand the natural history of aging. This will introduce the possibility of interventions to promote wellbeing and longevity across the lifecourse.

For example, our early research is showing differences in aging at the very beginning of life (in infancy) and also some of the factors that predict these differences.

Puberty also starts at varying ages and may set up early differences in biological aging. Puberty also has a major role in shaping our brains. Early or late puberty can have a profound impact on teenagers’ mental and physical health.

Differences in aging can emerge later in the lifecourse too, in young and middle adulthood. We are particularly interested in the role of mental health difficulties, traumatic life events and substance misuse in accelerating biological aging.

How our research compares biological and chronological aging

The molecular sciences research theme works to understand how a person’s social context can ‘get under the skin’ to shape brain systems related to social cognition, language and memory.

Our work includes advancing research in developmental epigenetics (expression of genes) as perhaps the key biological mechanism through which the environment can shape brain development.

We measure biological aging (your body’s age) as distinct from chronological aging (your calendar age). In teenagers, this can help us understand the impact of puberty on brain development independent of aging.

These new biometrics can feed into our SEED longitudinal and intervention studies, to better understand the social determinants of both accelerated and decelerated aging with respect to chronological age. We examine how experiences in the first half of the life course shape destinies in the second half, including earlier patterns of:

  • physical health (exercise, nutrition and sleep)
  • relationship quality (family and non-family social networks and support)
  • emotional regulation (prosocial behaviour, depression, anxiety, substance use)
  • social context (neighbourhood safety, resources and opportunities).

Our purpose is to provide biological informed reasons for government and community level investment in early life interventions that have the potential to both slow pace-of-aging and promote wellbeing across the lifecourse.

Our purpose


To advance research in developmental epigenetics as a key biological mechanism through which the environment shapes brain development.


To develop capabilities in our longitudinal cohort studies to enable new bioscience analyses.


To develop advanced algorithms for measuring biological aging as distinct from chronological aging.


To feed new biometrics into longitudinal and intervention studies for better understanding of the social determinants of accelerated and decelerated aging.

Our leaders

Tim Silk
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Peter Fransquet
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Craig Olsson
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