Revolutionary treatment could stop and reverse early-stage Alzheimer’s

In the battle against Alzheimer's disease, a team of researchers at the Technical University of Munich (TUM) has made significant strides with a promising new therapeutic approach. They have focused their efforts on a specific target: the amyloid-beta biomolecule.

This molecule is notorious for triggering the hyperactivity of nerve cells, which is a hallmark of the early stages of Alzheimer's. The team, led by Dr. Benedikt Zott and Prof. Arthur Konnerth from TUM's School of Medicine and Health, along with Prof. Arne Skerra from TUM's School of Life Sciences, has developed a protein drug that may suppress the harmful effects of amyloid-beta.

Their groundbreaking study, published in Nature Communications, shows promising results from laboratory experiments conducted on mice. These findings suggest that the neuronal dysfunctions caused by Alzheimer's could potentially be reversed. The researchers are hopeful that the protein they have developed, known as amyloid-beta-binding anticalin (H1GA), could stop the progression of Alzheimer's if administered at an early stage.

Globally, around 55 million people are living with dementia, with Alzheimer's being the most common form. Each year, approximately 10 million new cases of dementia are diagnosed, a staggering number that underscores the urgent need for effective treatments. Currently, there is no medication that can address the fundamental mechanisms of Alzheimer's disease. Treatments available today only manage symptoms, such as declining cognitive function, rather than tackling the disease itself.

Dr. Zott highlights the importance of their findings, stating, "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." This suppression of hyperactivity could be crucial in preventing the progression of Alzheimer's, offering hope for future treatments.

The development of H1GA involved advanced protein design techniques, with the team producing the active protein in genetically modified Escherichia coli bacteria. The drug was then administered directly into the hippocampus, the brain region most affected by Alzheimer's. Remarkably, after treatment, the previously hyperactive brain cells in mice were indistinguishable from healthy nerve cells, suggesting a reversal of the disease's effects.

However, the researchers acknowledge that there are still significant challenges ahead. It remains uncertain whether these promising results can be replicated in human patients outside of the controlled laboratory environment. Furthermore, the method of delivering the active ingredient directly to the brain is invasive, and the team is currently working on developing a more effective and less invasive form of administration.

It's worth noting that previous attempts to develop similar treatments have not been successful. For instance, in 2016, the drug solanezumab, which was designed to target amyloid-beta in a similar manner, failed in large-scale clinical trials.

The failure of solanezumab has been attributed to differences in its molecular structure compared to H1GA. In their study, Zott and his colleagues directly compared H1GA to solanezumab, with the new protein showing more pronounced positive effects, giving hope that H1GA might succeed where other treatments have fallen short.

This study is part of a broader research effort funded by the Albrecht Struppler Clinician Scientist Program at TUM. This program fosters collaboration between various departments, including the Department of Neuroradiology, the Institute of Neuroscience, and the Chair of Biological Chemistry. The funding has supported the research from the initial stages of protein biosynthesis to the first efficacy tests in animal models.

The researchers involved in this study are also part of the SyNergy Cluster of Excellence, a group dedicated to investigating complex neurological diseases like multiple sclerosis and Alzheimer's. The cluster employs an interdisciplinary approach known as systems neurology, which allows for a comprehensive mapping of the numerous processes involved in neurodegenerative, neuroimmunological, and neurovascular diseases.

The SyNergy Cluster has received funding from the Excellence Initiative of the German federal and state governments since 2012, reflecting the high level of commitment and investment in understanding and combating these debilitating conditions.

While the journey toward a viable Alzheimer's therapy for humans is still in its early stages, the work being done at TUM represents a significant step forward. If the results seen in mice can be replicated in humans, the impact on millions of people worldwide could be profound. The future of Alzheimer's treatment may well be shaped by these early, promising developments in protein-based therapies.

Note: Materials provided above by The Brighter Side of News. Content may be edited for style and length.

Like these kind of feel good stories? Get The Brighter Side of News' newsletter.