Stopping and reversing Alzheimer's at an early stage

TUM study shows promising therapeutic approach

19-Aug-2024

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In the fight against Alzheimer's, researchers at the Technical University of Munich (TUM) have developed a promising, preventative therapeutic approach. They specifically targeted the amyloid beta biomolecule, which triggers the hyperactivity of nerve cells typical of the brain disease in its early stages. The team led by Dr. Benedikt Zott and Prof. Arthur Konnerth from the TUM School of Medicine and Health and Prof. Arne Skerra from the TUM School of Life Sciences succeeded in developing and using a protein drug that can suppress the effects of the harmful molecule.

The results obtained on mice in the laboratory indicate that neuronal dysfunctions could even be repaired. The researchers hope that the protein they are investigating, which experts refer to as amyloid-beta-binding anticalin (H1GA), can halt the progression of the serious neurodegenerative disease in its early stages.

According to the Alzheimer's Society, there are around 1.8 million dementia patients in Germany, most of whom suffer from Alzheimer's disease. There is currently no medication to combat the basic mechanisms of the disease. Only symptoms such as declining mental performance can be treated.

Dr. Benedikt Zott emphasizes: "We are still a long way from a therapy that can be used in humans, but the results in animal experiments are very encouraging. The effect of completely suppressing neuronal hyperactivity in the early stages of the disease is particularly remarkable."

The researchers obtained the anticalin H1GA by protein design and produced it in genetically modified Escherichia coli bacteria. The active ingredient was injected directly into the hippocampus region of the brain. The previously hyperactive brain cells could then no longer be distinguished from healthy nerve cells in terms of measurable behavior.

It is still unclear whether the effect can actually be achieved in human patients outside the laboratory. In any case, a more effective form of administering the active ingredient is currently being developed. In 2016, the active substance solanezumab, which was supposed to have a similar effect, proved to be a failure in large-scale clinical trials, but this can be explained by its different molecular structure. Zott and his colleagues also compared their new active ingredient directly with solanezumab in the trials. H1GA showed clearer positive effects.

Note: This article has been translated using a computer system without human intervention. LUMITOS offers these automatic translations to present a wider range of current news. Since this article has been translated with automatic translation, it is possible that it contains errors in vocabulary, syntax or grammar. The original article in German can be found here.

Original publication

Benedikt Zott, Lea Nästle, Christine Grienberger, Felix Unger, Manuel M. Knauer, Christian Wolf, Aylin Keskin-Dargin, Anna Feuerbach, Marc Aurel Busche, Arne Skerra, Arthur Konnerth; "β-amyloid monomer scavenging by an anticalin protein prevents neuronal hyperactivity in mouse models of Alzheimer’s Disease"; Nature Communications, Volume 15, 2024-7-10

https://www.bionity.com/en/news/1184208/stopping-and-reversing-alzheimer-s-at-an-early-stage.html