A method that could stop the growth of Alzheimer’s disease in the early stages of development has been discovered. Scientists consider this breakthrough the potential future of Alzheimer’s disease treatments, allowing for a new wave of inhibitor molecule drug discovery treatments types.
A research team at Cambridge University, in collaboration with partners in Estonia and Sweden, has identified a naturally occurring biological inhibitor molecule that can slow the formation of plaques in the brain, and potentially block the growth progress of Alzheimer’s at a integral stage in its development.
This breakthrough is the first of it’s kind, providing a path to break the cycle leading to the development of Alzheimer’s in the brain. Scientists also believe that this technique can be used to locate and define other inhibitor molecules as future treatments for different disease stages.
The discovery and its implications are published in the journal Nature Structural & Molecular Biology. Lead author Dr. Samuel Cohen explains “A molecular chaperone has been found to inhibit a key stage in the development of Alzheimer’s disease and break the toxic chain reaction that leads to the death of brain cells.” Cohen, a research fellow at St John’s College in Cambridge says studies like this are the rewards of years of extensive work done to increase our understanding of the microscopic processes involved in the development of Alzheimer’s.
“Our study shows, for the first time, one of these critical processes being specifically inhibited, and reveals that by doing so we can prevent the toxic effects of protein aggregation that are associated with this terrible condition.”
Alzheimer’s is the top disease leading to dementia and occurs slowly over time as malfunctioning proteins in the brain develop amyloid plaque deposits that form into amyloid fibrils. Amyloid fibrils are the hallmark of Alzheimer’s disease, and are closely associated with declining memory and other Alzheimer’s symptoms.
The inhibitor molecule, called Brichos, sticks to the amyloid fibrils to stop these threads from coming into contact with other proteins, limiting the formation of highly toxic clusters that enable the condition to proceed to the second stage marked by proliferation in the brain and hastening of the most devastating Alzheimer’s symptoms.
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