The brain has its own unique defence system, which responds to damage and infection. Prof Clare Bryant, who also works as vet, has a keen interest in applying biological processes she has learnt about in animals to diseases experienced by people. She is fascinated by the role of a particular type of brain defence cell, known as microglia. Microglia act like hoovers, removing waste that builds up normally in the brain as well as the toxic proteins that build-up in Alzheimer’s and other forms of dementia, including dementia with Lewy bodies. This is vital for protecting nerve cells from damage. However, the inflammatory response of microglia to nerve cell damage in Alzheimer’s is as complicated as the disease itself. When microglia are active for a prolonged period of time, as in Alzheimer’s, researchers believe these cells may in fact switch roles and start to cause nerve cell injury. Prof Bryant wants to understand more about these different microglial responses.
Prof Bryant’s innovative research will aim to shed light on a potential avenue for treatment. Targeting the microglia response may prove to be a way to dampen brain inflammation and reduce nerve cell damage in Alzheimer’s and dementia with Lewy bodies. Prof Bryant is new to dementia research, but the application of her vast knowledge of inflammation from the veterinary world, in collaboration with experts from the University of Cambridge, will provide us with new insights into the brain changes in Alzheimer’s disease and dementia with Lewy bodies.
Prof Bryant will study a protein called Toll-like receptor 4 (TLR 4). TLR 4 communicates information from the brain environment into microglial cells. Prof Bryant believes that TLR 4 senses different forms of amyloid – the protein that builds-up in Alzheimer’s – and causes microglia to respond to damage. By using sophisticated microscopes, Prof Bryant will be able to look at the interactions between amyloid clumps of varying sizes and TLR4 to understand what prompts the prolonged microglial response.
Prof Claire Bryant
University of Cambridge
1 September 2014 - 31 January 2018
Full project name
The molecular basis of the innate response to oligomers of beta amyloid and alpha synuclein