The link between amyloid plaques and atherosclerosis

The mechanism and cellular effects of apolipoprotein A-I aggregation into amyloid fibrils associated with atherosclerosis

David Middleton (lead researcher)

Lancaster University

Start date: 01 October 2013 (Duration 3 years)

Atherosclerosis is a potentially fatal condition in which the arteries supplying the heart become clogged by fatty plaques, causing coronary heart disease. High blood levels of LDL ‘bad’ cholesterol increase the risk of coronary heart disease as they build up in the inner walls of the arteries. High blood levels of HDL ‘good’ cholesterol on the other hand seem to protect against atherosclerosis by removing cholesterol from the arteries. Research has shown that a protein called apolipoprotein A-I (apoA-I), which is part of the HDL complex, can itself accumulate in atherosclerotic plaques in the form of amyloid, a substance that is also found in the brain of patients with Alzheimer’s disease. The consequences of apoA-I amyloid deposition is not clear, but it might contribute to atherosclerosis by lowering the blood levels of good cholesterol or by increasing the size of the plaques or even by damaging the artery walls. This PhD studentship at Lancaster University aims to find out how apoA-I forms these amyloid plaques and how they affect the cells that make up the artery walls.

Project details

Grant amount £104,305
Grant type Fellowship
Application type PhD Studentship
Start Date 01 October 2013
Duration 3 years
Reference FS/13/28/30208
Status Complete

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