Alzheimer’s Breakthrough: New Study Reveals Reversal and Prevention

Alzheimer's disease affects millions worldwide, wherein memory and thinking skills are destroyed. It's thought to start with amyloid plaques in the brain. Now, however, researchers at the Technical University of Munich have discovered a smaller and more hidden culprit—amyloid beta monomers, or Aβ—which could be the real cause.

This might prevent Alzheimer's from occurring before it develops. The small protein parts, known as Aβ monomers, enlarge themselves and aggregate to cause damage to the brain.

They are the building blocks of the larger amyloid plaques, but even before these large plaques form, Aβ monomers alone can do damage. This discovery offers new ways to treat Alzheimer's.

Others have focused on the bigger amyloid plaques that come later, but experts now turn attention to how to hit Aβ monomers developing in the early stages of Alzheimer's. In order to fight these monomers, they came up with a protein fiber called an anticalin.

The anticalin H1GA works like a sponge, soaking up harmful Aβ monomers before they reach dangerous levels.

The researchers are trying to prevent Alzheimer's from developing by preventing these monomers clumping together. They employ anticalin early to prevent the disease and enhance recovery.

However, anticalin is not available for humans yet; they are going to test it on rats first. The tests turned out quite well and proved satisfactory. Researchers observed brain activity in live mice.

They injected the Aβ-anticalin directly into the hippocampus—a central area of the brain responsible for memory and learning—in mice genetically engineered to develop Alzheimer's.

Results were stunning: Aβ-anticalin strongly reduced excessive, overstimulating neuronal activity the researchers saw in Alzheimer's mice. This hyperactivity is considered an early warning for the disease.

The anticalin kept brain cells functioning normally by preventing the Aβ monomers from clumping together and thus effectively halting this early damage. While human trials are a long way off, the finding offers hope and reveals a promising new approach for treating Alzheimer's.

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