Alzheimer’s disease affects millions of people around the world. This notorious disease impairs cognitive abilities and destroys precious memories. The disease is caused by the accumulation of amyloid plaques in the brain. However, a remarkable study by scientists at the Technical University of Munich (TUM) reveals that the cause is a more insidious and tiny threat – the amyloid beta monomer (Aβ).
By targeting this early, it may be possible to stop this devastating disease before it even starts. The tiny protein fragments grow and clump together, wreaking havoc in the brain. They form the basis for the larger amyloid plaques. Even before the plaques develop, Aβ monomers pose a significant threat, causing damage of their own. The new origin has opened up new avenues for treating Alzheimer’s.
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Targeting the real cause
Previously, the focus was on amyloid plaques that form later in the disease process. But now researchers are shifting their treatment target to targeting the Aβ monomers that develop early in the disease. To counteract the monomers, researchers created a protein fiber called anticalin.
Anticalin, also called H1GA, acts like a molecular sponge, absorbing the dangerous Aβ monomers before they reach worrying levels. By preventing these monomers from clumping together, researchers hope to prevent Alzheimer’s from setting in. By taking the necessary precautions in the early stages with Anticalin, researchers hope to prevent Alzheimer’s. Changing the focus of treatment will also contribute to a better recovery.
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Still a long way to go
However, Anticalin is not available for humans and is currently being tested on rats. The test results were as expected and were successful. The researchers monitored brain activity in living mice. They administered Aβ-Anticalin directly into the hippocampus, an important brain region for memory and learning, of mice that had been genetically modified to develop Alzheimer’s disease.
The results were impressive, as the Aβ anticalin significantly reduced excessive, overstimulating neuronal activity in mice suffering from Alzheimer’s disease. This hyperactivity is perceived as an early warning sign of the disease. By preventing the formation of harmful clumps by Aβ monomers, the anticalin effectively stopped this early damage and maintained normal brain cell function. Although there is still a long way to go before human trials, this finding is hopeful and opens up a better avenue for treating Alzheimer’s disease.
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