Researchers at the Technical University of Munich (TUM) have made significant advancements in the prevention of Alzheimer’s disease. They have particularly focused on the amyloid beta biomolecule, known for causing excessive activity in nerve cells, which is common in the early stages of the disease. The team, led by Dr. Benedikt Zott and Prof. Arthur Konnerth from the TUM School of Medicine and Health, along with Prof. Arne Skerra from the TUM School of Life Sciences, has successfully created and applied a protein drug designed to counteract the adverse effects of this harmful molecule.
Laboratory tests on mice suggest that it may even be possible to repair certain neuronal dysfunctions. Their findings were published in the journal Nature Communications. The researchers are optimistic that the protein they studied, called amyloid-beta-binding anticalin (H1GA), has the potential to slow down the early progression of this severe neurodegenerative illness.
Experts estimate that around 55 million individuals worldwide are currently living with dementia, with a significant majority diagnosed with Alzheimer’s. Approximately 10 million new cases arise each year. At present, no drugs exist to tackle the fundamental mechanisms of the disease, with treatment options only addressing symptoms like cognitive decline.
Dr. Benedikt Zott points out: “While we are still far from having a therapy ready for human use, the outcomes from our animal studies are very promising. It’s especially noteworthy to observe a complete suppression of neuronal hyperactivity in the disease’s early stages.”
The team engineered the anticalin H1GA through protein design, producing it using genetically modified Escherichia coli bacteria. This active compound was then administered directly to the hippocampus in the brain. Following treatment, the previously hyperactive brain cells behaved similarly to healthy nerve cells in measurable ways.
It remains uncertain whether these effects can be replicated in human patients outside of laboratory conditions. Meanwhile, a more effective method for administering the active ingredient is currently under development. In 2016, solanezumab, a substance intended to achieve similar results, failed in large clinical trials; this was attributed to its differing molecular structure. Zott and his team directly compared their new drug to solanezumab during trials, and H1GA demonstrated more pronounced positive results.
