New research has shown that it may be possible to control the mechanism that leads to the rapid build-up of amyloid plaques which are a key hallmark of Alzheimer's disease.
The study published today (Monday 18 July) in the journal, Nature Physics, was carried out by researchers from the Department of Chemistry at the University of Cambridge.
Using computer simulations the researchers explored the requirements for amyloid proteins to assemble into fibrils, the core component of amyloid plaques. They identified a critical step in the process where normal amyloid proteins accumulate on the surface of existing protein fibrils and then become fibrils themselves. As a proof of principle, the research shows that by changing how healthy amyloid proteins interact with the surface of amyloid fibrils, it is possible to slow down the rate at which new amyloid fibrils are produced.
Dr James Pickett, Head of Research at Alzheimer's Society said:
'Reducing the build-up of amyloid plaques in the brain, the hallmark of Alzheimer's disease, is a key focus of several current clinical trials. However, there is an ongoing debate among scientists about which step in the process of amyloid plaque formation should be the target for drug treatments.
'Today's study brings more useful evidence to these discussions by using computer modelling to examine the interactions between amyloid proteins and predict what is happening in the brain of a person with Alzheimer’s when plaques are formed. The next step is for these predictions to be tested in living cells so that the information can usefully help in the design of more effective treatments to target amyloid.'