Mechanism Behind Alzheimer's Disease Discovered

Amyloid fibrils rapidly self-replicate in Alzheimer’s disease.

The mechanism that leads to amyloid plaques, a characteristic of Alzheimer’s disease, were discovered in a new study.

Certain protein structures, called fibrils, can replicate without additional assistance. Amyloids are fibrils and can replicate this way.

When amyloids intertwine with each other, they cause plaques found in the brains of patients with Alzheimer’s disease, according to the study published in Nature Physics.

The formation of the initial amyloid fibrils takes decades, but the process is much more rapid following the initial formation. But, the process these fibrils can replicate without additional assistance is not fully understood.

In the study, researchers used computer simulations and experiments to discover how fibrils self-replicate. The researchers discovered the process is governed by the build-up of healthy proteins on the surface of existing fibrils.

They used amyloid-beta, the main component of the amyloid plaques, to discover this relationship. The healthier the proteins deposited, the faster the fibrils self-replicated.

Their findings suggest that fibril self-replication could potentially be controlled through changing the interaction between healthy proteins and the surface of existing fibrils.

“One of the mysteries of amyloid plaque formation is how, after their long, slow formation, the speed of their progression becomes much faster,” said the study's first author Andela Saric, PhD. “We've identified the factors that in fact cause the system to catalyze its own activity, becoming a runaway process. But this discovery suggests that if we're able to control the build-up of healthy proteins on the fibrils, we might be able to limit the aggregation and spread of plaques.”

The researchers also believe their findings could be used to further nanotechnology.

“One of the unfilled goals in nanotechnology is achieving efficient self-replication in manufacturing of nanomaterials,” concluded Dr Saric. “This is exactly what we've observed happening with these fibrils -- if we're able to learn the design rules from this process, we may be able to achieve this goal.”