Dr Nathan Woodling

Lecturer (Molecular Biosciences)

telephone: 0141 330 8299
email: Nathan.Woodling@glasgow.ac.uk
pronouns: He/him/his

Davidson Building 241, University of Glasgow, Glasgow, G12 8QQ

Biography

Nathan completed his PhD in 2013 at Stanford University, where he studied the way that inflammatory signalling pathways in microglia contributed to the types of neurotoxicity seen in Alzheimer’s disease. He then moved to the UCL Institute of Healthy Ageing for his postdoctoral work, which investigated how both glial and neuronal cells can modulate ageing of the nervous system through different signalling pathways. In 2019, he was awarded an Alzheimer’s Society Junior Fellowship, which allowed him to investigate how age-related changes in glia may predispose the nervous system to the types of damage that occurs in Alzheimer’s disease. In 2022, Nathan moved to Glasgow to start his own research group investigating how specific cell signalling pathways modulate ageing and the age-related susceptibility to neurodegenerative diseases.

Research interests

The Woodling Lab aims to understand the evolutionary origins and biological underpinnings of ageing. Our goal is to discover genes and proteins that can be targeted to extend the time of life spent in disease-free good health.

To work towards this ambitious goal within a lab setting, we primarily use the fruit fly Drosophila, whose genetics and ageing trajectory are remarkably well shared with those in humans. Working with flies allows us (a) to study ageing at 300 times the speed of a human lifespan and (b) to manipulate gene expression in specific tissues to determine how individual signalling pathways affect healthy longevity in organ-specific ways.

Equally important, our lab aims to be a place of curiosity-driven discovery where each team member can flourish at their full potential. This means a continual development and re-development of our approaches grounded in our values of collegiality, integrity, and inclusion.

Our current research questions include:

How do developmental processes contribute to ageing?

One prominent evolutionary theory predicts that ageing is the consequence of developmental run-on, or the continued activity of signalling pathways essential in early life but detrimental in late life. A well-studied example is the insulin/ insulin-like growth factor signalling (IIS) network, where studies in animals as diverse as worms, flies, and mice have shown that IIS inhibition can extend healthy longevity. Some of our own work has shown that this effect extends to other receptor tyrosine kinases closely related to the insulin receptor but expressed in distinct tissues. We now aim to investigate how other related receptors and signalling pathways can modulate healthy longevity, using flies as our discovery platform.

How do genetic background and sex differences affect ageing?

Even in organisms as seemingly simple as flies, major differences in ageing trajectories are seen between sexes and among different genetically isolated strains. For instance, some of our recent work has found stark differences (and some similarities) in the ways that ageing affects sleep and activity patterns in female and male flies from different laboratory strains. We now aim to discover the biological mechanisms underlying these behavioural changes with age, as well as whether these mechanisms are shared among sexes and strains.

How do ageing-related signalling pathways affect the pathogenesis of age-related diseases?

We ultimately aim to uncover biological mechanisms that can extend the time of life spent in good health while also preventing or delaying the onset of age-related diseases. We therefore have tested some of our findings in fruit fly models of the toxic proteins that cause some major diseases of ageing. For instance, one of the transcription factors we studied in neurons can also protect flies against the effects of Amyloid-beta, a peptide thought to initiate toxic cascades in Alzheimer’s disease. We now aim to test additional ageing-related genes and signalling pathways for their potential to protect against models of age-related diseases.