Investigating the brain cell sub-types that modulate healthy ageing in response to diet and nutrient-sensing signalling pathways
Supervisors
Dr Nathan Woodling, School of Molecular Biosciences, University of Glasgow
Dr Susan Broughton, Division of Biomedical and Life Sciences, Lancaster University
Summary
Why do we age? The answer to this question will be fundamental to discovering interventions that can prolong the amount of life spent in disease-free good health. Although science still lacks a consensus answer, recent work has discovered specific cell signalling pathways that modulate ageing across animal species. For instance, genetic manipulations that reduce insulin-like signalling can extend lifespan in species as diverse as fruit flies and mice, and it can also prolong the period of life in which these animals remain in good health, or ‘healthspan’. Recent work from the Woodling and Broughton labs has used the short lifespan and genetic toolsets in the fruit fly Drosophila to show that many of the same effects can be seen even when these genetic manipulations are targeted to specific brain cell types such as serotonergic neurons or astrocyte-like glial cells.
This project will build on these previous studies to discover how insulin signalling in such small cell populations affects lifespan and healthspan. The project will use a wide array of techniques including Drosophila functional genetics, survival and behavioural analysis, and single-cell transcriptomic analysis – thus providing training opportunities not only in lab-based neurobiology and gerontology techniques but also in coding and computational analysis of big data.