Identifying targets to tackle brain inflammation

Researchers at King’s Collage London are investigating potential drugs to stop damaging inflammation in brain cells.

Researching

Treatments

Inflammation is thought to contribute to damage to nerve cells in Alzheimer’s disease. Drugs that could reduce levels of brain inflammation are an important avenue of research towards new treatments for the disease. In this project Dr Wendy Noble will study the role of a protein that is thought to regulate inflammation in Alzheimer’s and explore whether blocking this protein could help limit damage to nerve cells in the disease.

Alzheimer’s is a multifaceted disease which involves a number of different brain changes that combine to cause damage to nerve cells. While build up of the proteins amyloid and tau are the most studied of these brain changes, recent research has highlighted the important role of inflammation. To have the best chance of developing effective new treatments, researchers need to explore ways to tackle all these harmful processes involved in the disease.

Dr Wendy Noble and her team at King’s Collage London have identified a protein, called P2X7, that helps regulate inflammation in Alzheimer’s. They hope that by learning more about its role, and carefully examining the effects of blocking its action, they could pave the way to future treatments that limit harmful brain inflammation, protect nerve cells and improve the lives of people with Alzheimer’s.

Previous experiments by the team indicate that the P2X7 protein has a role in increasing inflammation that damages brain cells. To verify that the protein plays a role in Alzheimer’s, they will measure levels of the P2X7 in brain tissue donated by people with Alzheimer’s disease compared to that from people who died without the disease.

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Awarded to
Dr Wendy Noble

Institution
King's College London

Current Award
103,859.40

Dates
1 October 2018 - 30 September 2021

Full project name
Investigating P2X7-mediated inflammatory signalling in Alzheimer’s disease