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Computer modelling sheds light on Alzheimer's

New research puts scientists a step closer to tackling the degenerative disease 
Amyloid fibrils

Researchers from the University of Cambridges department of chemistry have shown that it may be possible to control the mechanism that leads to the rapid build-up of amyloid plaques a hallmark of Alzheimers disease.

Amyloid fibrils, a key component of amyloid plaques which are a hallmark of Alzheimer's disease. Photo: SPL

The researchers used computer simulations to explore 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 fibres and then become fibrils themselves.

The research showed 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.

Alzheimers Society research shows that 850,000 people in the UK have a form of

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Researchers from the University of Cambridge’s department of chemistry have shown that it may be possible to control the mechanism that leads to the rapid build-up of amyloid plaques – a hallmark of Alzheimer’s disease. 


Amyloid fibrils, a key component of amyloid plaques which are a hallmark of Alzheimer's disease. Photo: SPL

The researchers used computer simulations to explore 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 fibres and then become fibrils themselves. 

The research showed 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. 

Alzheimer’s Society research shows that 850,000 people in the UK have a form of dementia. The organisations’ head of research James Pickett said: ‘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.’ 

Šarić A et al (2016) Physical determinants of the self-replication of protein fibrils. Nature Physics. doi: 10.1038/nphys3828

 

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