Computer model maps spread of toxic Alzheimer’s protein

Researchers in Canada have used a computer model to try to map the spread of toxic proteins involved in Alzheimer’s disease.

Posted on 20th November 2014

Researchers in Canada have used a computer model to try to map the spread of toxic proteins involved in Alzheimer’s disease. The study is published on Thursday 20 November in the journal PLOS Computational Biology and can be read online here.

The team at the Montreal Neurological Institute focused on a protein called amyloid, which is involved in Alzheimer’s disease, the most common cause of dementia. Although amyloid is present in healthy brains, in Alzheimer’s the protein ‘misfolds’ and begins to accumulate, clumping together around nerve cells. This build-up of misfolded, toxic amyloid is thought to trigger the disease.

The researchers looked at images from brain scans of 733 people who were part of the Alzheimer’s Disease Neuroimaging Initiative (ADNI), which showed different stages of amyloid build-up in the brain. Using a computer model that was originally designed to simulate the spread of epidemic diseases across the globe, they looked for patterns that could explain how amyloid spreads from one part of the brain to another.

Their results showed that within the brain, the protein seemed to spread in a pattern that was similar to the way epidemics spread from one region to another. The computer model suggested that toxic proteins may spread through connections in brain networks, which join different regions of the brain to one another – much as connecting hubs in air traffic networks can play a role in the spread of infectious diseases.

The researchers also used the model to investigate the effects of amyloid production and clearance rates. In their model, the rate at which amyloid was cleared from the brain could affect the build-up of the protein – suggesting that problems with the brain’s clearance mechanisms may also play a part in the disease.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“The build-up of amyloid is one of the first changes seen in the brain in Alzheimer’s, but why the protein accumulates and what causes it to spread through the brain is still not fully understood. Growing evidence suggests that the protein may spread through brain networks and this useful study adds weight to this theory. Computer modelling can be a helpful tool for trying to predict the course of Alzheimer’s, but other methods are also needed to confirm how findings like these relate to the disease in the real world.

“Currently half a million people are living with Alzheimer’s in the UK, and we must invest in research if we are to find ways to treat the disease. A better understanding of the way the disease develops could bring vital new clues for producing treatments that could stop it in its tracks.”

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