A study from TUM demonstrates a promising therapeutic approach.

Researchers at the Technical University of Munich (TUM) have made promising advances in preventing Alzheimer’s by developing a new therapeutic strategy. Their approach focuses on targeting the amyloid beta biomolecule, known to cause the early-stage hyperactivity of nerve cells characteristic of the disease.

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 study was published in the renowned journal Nature Communications. The researchers hope that the protein they investigated, which experts refer to as amyloid-beta-binding anticalin (H1GA), can halt the progression of the serious neurodegenerative disease at an early stage.

Alzheimer’s Disease: A Growing Global Health Crisis

According to experts, there are an estimated 55 million people worldwide living with dementia, most of them suffering from Alzheimer’s. Each year, around 10 million new cases are diagnosed. 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 Development and Testing of H1GA

The researchers obtained the anticalin H1GA by protein design and produced it in genetically modified bacteria of the species Escherichia coli. 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 administration of 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.

Reference: “β-amyloid monomer scavenging by an anticalin protein prevents neuronal hyperactivity in mouse models of Alzheimer’s Disease” by Benedikt Zott, Lea Nästle, Christine Grienberger, Felix Unger, Manuel M. Knauer, Christian Wolf, Aylin Keskin-Dargin, Anna Feuerbach, Marc Aurel Busche, Arne Skerra and Arthur Konnerth, 10 July 2024, Nature Communications.
DOI: 10.1038/s41467-024-50153-y

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