Alzheimer’s disease develops over decades.
It begins with a fatal chain reaction in which masses of misfolded beta-amyloid proteins are produced that in the end literally flood the brain.
In a new study, researchers found that this chain reaction could start much earlier than commonly assumed.
This means that in addition to the well-known early phase of the disease with protein deposits but without symptoms of dementia, there is an even earlier phase in which the chain reaction is triggered by invisible tiny seeds of aggregation.
If this is confirmed to occur also in humans, a treatment addressing the causes of disease would have to prevent this process.
The scientists have already identified an antibody that might accomplish this.
The research was conducted by a team from the Hertie Institute for Clinical Brain Research (HIH) in Tübingen and elsewhere.
Although research on Alzheimer’s has been dealing with seeds of aggregation for quite some time, nobody really knows what they look like.
They are currently only defined by their role as triggers for this fatal chain reaction.
In the study, the team searched among the already known antibodies directed against misfolded beta-amyloid proteins for antibodies that can recognize and possibly also eliminate these early seeds of aggregation.
Of the six antibodies investigated, the only aducanumab had an effect: mice that were treated for only five days before the first protein deposits manifested, later on in life showed only half of the usual amount of deposits in their brains.
They were able to show that aducanumab recognizes protein aggregates, but not individual beta-amyloid chains.
The scientists hope to use the antibody as a fishhook to isolate and better describe these seeds of aggregation.
The new studies suggest that a treatment of Alzheimer’s that addresses the causes should start much earlier.
One author of the study is Mathias Jucker.
The study is published in Nature Neuroscience.
Copyright © 2020 Knowridge Science Report. All rights reserved.
