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Scientists discover why there’s a rapid build up of amyloid plaques in the Alzheimer brain

Researchers from the University of Cambridge have just completed a study which may help us to understand more about the mechanism underlying the rapid build up of amyloid proteins in people with Alzheimer’s. Furthermore, they believe that it may be possible to control this mechanism.

The foundation of life is dependent on the ability of our biological molecules to replicate themselves. This is can often be a difficult process involving complex cellular machinery. However, certain protein structures do appear to have the ability to replicate without any such complexities, including the small disease-causing fibrils (protein fibres) or amyloids normally associated with neurodegenerative disorders such as Alzheimer’s and Parkinson’s. These fibrils become entangled with each other to cause the ‘plaques’ that are present in the brains of people with Alzheimer’s. As the formation of the first plaques is very slow, usually taking several decades, this explains why it’s seen as a disease that affects older people. However, once the fibrils are formed, they replicate rapidly and start to spread. And it’s this rapid replication that makes the disease so difficult to control.

Until this recent study, why and how these protein fibrils replicate so quickly has not been very well understood. To learn more about the mechanisms underlying this process, the team from the University of Cambridge utilised computer simulations alongside experiments in the laboratory to discover what was needed in order for the protein fibrils to self-replicate. They found that rather than it being a very complicated process, it was actually controlled by a simple physical mechanism: the existing fibrils were able to replicate due to a build-up of healthy proteins on their surface.

By examing amyloid beta molecules, the researchers were able to find a correlation between the amount of healthy protein deposited onto the fibrils and the rate at which the fibril could self-replicate. They were also able to demonstrate in principle that if the way in which the healthy proteins interacted with the fibrils was changed, it would be possible to control the self-replication of the fibrils.

This study has proved very interesting as, until now, the speed at which fibrils replicated was very much a mystery, particularly as it took them so long to form. Now, having identified the factor that causes the increase in self-replication, it suggests that it will be possible to control the build up of the healthy proteins and thus limit the growth and spread of the amyloid plaques.

The results of the study are due to be published in the online journal Nature Physics.

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