Prions are a type of protein that can induce normal proteins in the brain to fold abnormally, leading to cellular death and the development of prion diseases, also known as transmissible spongiform encephalopathies (TSEs). Prions are infectious proteins that are devoid of any genetic material, making them different from bacterial and viral infectious diseases. Prion diseases affect both humans and animals and can be zoonotic as shown by the transmission of bovine spongiform encephalopathy (BSE) causing variant Creutzfeldt-Jakobs disease (vCJD) in humans.

Primarily using histopathology and related molecular biological techniques I aim to determine exactly how prions infect a host and eventually cause neurodegeneration. Due to their infectious nature, prions provide a tractable and well-characterized neurodegeneratve system within which we can interrogate the roles of various cell types, molecules and pathways involved in brain health and disease by for example the use of transgenic models. My ultimate goal is to cure prion disease and prevent neurodegeneration. Similarly we use prions alongside other infection models such as bacteria or parasites to determine the impact on host susceptibility or resistance to prion infection as well as impact on the disease course.

My major research findings have established and defined specific roles of various supporting cells within the brain called glia. I have identified unique signatures for each prion strain of agent and host response through upregulated expression of the adhesion molecule CD44 by astrocytes. I have also definitifely proven the neuroprotective nature of microglia by characterising the response of completely microglia-deficient animals to prion disease.

During my research I have also gained extensive experience of visualising and defining immune structures and responses in host animals and translating these techniques across a broad range of species including both commercial (cattle, sheep, poultry, pigs & salmon) and companion (dogs & cats) animals.