New study finds a breakthrough treatment to reverse Alzheimer’s disease

Alzheimer’s disease affects millions across the globe. This infamous disease impairs cognitive abilities and corrodes precious memories. The disease originates from the buildup of amyloid plaques in the brain. However, a noteworthy study by scientists at the Technical University of Munich (TUM) unveils the cause to be a more stealthy and tiny menace – amyloid beta (Aβ) monomer.
If this is targeted early on, it has the potential to stop this devastating disease in its tracks before it even begins. The tiny protein fragments grow and clump together to unleash chaos on the brain. They are the foundation of the bigger amyloid plaques. Before the plaques even develop, Aβ monomers pose a significant threat and cause damage by themselves. The new origin has opened up new avenues for treating Alzheimer’s.
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Earlier, the primary focus was concentrated on amyloid plaques that form later in the prognosis. But now, the researchers are shifting their treatment target to combat the Aβ monomers, which develop at the early stage of the disease. To counter the monomers, researchers prepared a protein fibre called an anticalin.
The anticalin, also named H1GA, behaves like a molecular sponge, absorbing the dangerous Aβ monomers before they transition into concerning levels. By stopping these monomers from clumping together, the researchers aim to prevent Alzheimer’s from taking hold. By taking necessary precautions at the initial stages with anticalin, the researchers hope to prevent Alzheimer’s. The change in the treatment’s focus will also assist in better recovery.
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However, anticalin is not available for humans and is currently being tested on rats. The test result met the expectations and ran successfully. The researchers monitored the brain activity in live mice. They administered the Aβ-anticalin directly to the hippocampus, an important brain region for memory and learning, in mice genetically engineered to develop Alzheimer’s disease.
The results were impressive as the Aβ-anticalin substantially reduced excessive, overstimulating neuronal activity in Alzheimer’s-affected mice. This hyperactivity is perceived as an early warning sign of the disease. By preventing Aβ monomers from forming harmful clumps, the anticalin effectively stopped this early damage and maintained normal brain cell function. Despite a long way to go for human trials, this finding is hopeful and uncovers a better treatment pathway for Alzheimer’s.
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