Investigating the role of membrane interactions in the aggregation and toxicity of amyloidogenic proteins affecting the heart and vasculature

Award Number
Project Grant
Status / Stage
17 October 2016 -
17 October 2018
Duration (calculated)
02 years 00 months
British Heart Foundation (BHF)
Funding Amount
Funder/Grant study page
British Heart Foundation
Contracted Centre
Lancaster University
Principal Investigator
Professor David Middleton
PI Contact
WHO Catergories
Understanding Underlying Disease
Disease Type
Alzheimer's Disease (AD)

CPEC Review Info
Reference ID593
ResearcherReside Team


Award NumberPG/16/18/32070
Status / StageCompleted
Start Date20161017
End Date20181017
Duration (calculated) 02 years 00 months
Funder/Grant study pageBritish Heart Foundation
Contracted CentreLancaster University
Funding Amount£147,192.00

Plain English Summary

Professor David Middleton and his colleagues at Lancaster University are studying how proteins called amyloid build up in the heart and circulatory system, having potentially devastating effects on health. In several diseases, proteins clump together to form deposits called amyloid that builds up in organs. In Alzheimer’s disease, amyloid plaques accumulate in the brain. Amyloid protein can also affect the heart and circulatory system – it is deposited in the arteries of virtually everyone over the age of 50, and scientists think this increases the risk of aneurysms (bulging of the blood vessels) in older people. Scientists have discovered that the amyloid protein found in Alzheimer’s disease interacts with the outside layer of brain cells, causing the protein to clump together more quickly and then damage the cells. In this project, Professor Middleton’s team will study two proteins that form amyloid in the heart and blood vessels, and investigate whether they too interact with the outer layers of cells and clump together to form amyloid, destroying cells and affecting the heart and blood vessels. They will also investigate whether these amyloid proteins damage or destroy the cells by making them leaky. This work will help us to understand what causes amyloid diseases that affect the heart and blood vessels and could help eventually develop new treatments.