About the project
Alzheimer’s disease (AD) is a neurodegenerative disease, with a complex biology. In this PhD project, we aim to explore the cellular and molecular mechanisms underlying accelerated tau pathology following a systemic bacterial infection. The results may lead to improved understanding of the biological mechanism underlying spreading of tau in the AD-affected brain.
Build-up of ‘plaques’ in the brain is recognised as an early feature of Alzheimer’s disease. Scientists have discovered other factors, such as the presence of tau tangles and inflammation better predict memory loss. Tau tangles can spread through the brain affecting a whole network of neurons. Using an experimental model of AD, we showed that a systemic infection speeds up the spreading of tau, possibly due to activation of microglial cells.
This PhD studentship aims to explore the cellular and molecular mechanisms underlying accelerated tau pathology following a systemic infection. You will use a mouse model and human AD tissue to study the effect of a real live, systemic infection on glial activation, tau pathology and amyloid load. Using a range of advanced molecular techniques, you will investigate how glial cells and neurons interact and organise across the tissue landscape. By exploring different time points you will aim to identify when different cell types contribute to the spreading of tau. Bacterial infections can be treated, so understanding the connection to the brain may lead to novel treatment of and outcomes for AD patients.
You will benefit from training in a range of techniques, including:
- in vivo models
- histology
- advanced imaging
- spatial transcriptomics
- computational modelling
External supervisor
Alongside Professor Jessica Teeling, you will be supervised by Professor Katie Lunnon.