Drug stops Alzheimer's in mice

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Hope for Alzheimer's patients - disease in mice stopped

The number of Alzheimer's diseases will rise significantly across Germany in the coming decades. Research into possible therapies for the previously incurable neurodegenerative disease is therefore under way. A team of researchers from the Charité – Universitätsmedizin Berlin, the University of Zurich and the Humboldt University in Berlin has now successfully tested a new approach to treating Alzheimer's in experiments with mice and published the results in the journal “Nature Medicine”.

"By blocking a messenger substance of the immune system, the changes typical of the disease in Alzheimer's mice could be significantly reduced," said the Berlin Charité on the latest research results. The new treatment approach promises clear success in both prevention and therapy of the already manifested disease, the researchers report. By blocking a special messenger substance, the deposition of the typical protein plaque from amyloid-beta in the brain of Alzheimer's mice could be significantly reduced and the animals showed a significant improvement in their memory, write the scientist under Professor Frank Heppner from the Institute for Neuropathology at the Berlin Charité and Professor Burkhard Becher from the Institute for Experimental Immunology at the University of Zurich.

Deposition of Alzheimer's plaques significantly reduced According to the researchers in Germany and Switzerland, around 1.5 million people suffer from Alzheimer's. The number of patients worldwide is expected to double in the next 20 years. New treatment approaches for the previously incurable disease are therefore urgently needed. The scientists were now able to demonstrate that “switching off certain messenger substances in the immune system, so-called cytokines, which also include the interleukins, significantly reduces the amyloid beta deposits in Alzheimer's mice.” The effect was particularly pronounced when interleukins 12 and 12 were blocked The researchers report 23 (IL-12; IL23), which both contain the immune molecule p40. Mice that had no docking sites for p40 or were unable to produce the immune molecule at all showed a reduction in “amyloid-β of around 65 percent,” according to the Berlin Charité.

Improvement of memory in Alzheimer's mice In subsequent experiments, the researchers found that even with existing Alzheimer's disease, a clear improvement can be achieved by blocking the immune molecule p40. They injected p40 blocking antibodies into the bloodstream or brain. While the injection into the blood had no significant effect, the mice showed a significant improvement in memory when the antibodies were administered to the brain in behavioral tests, the scientists report. The level of the p40 molecule in the cerebral fluid and in the blood plasma is also increased in people with Alzheimer's disease, so that relevance for therapy in humans is obvious. Analysis of the brain fluid of 39 Alzheimer's patients and 20 healthy volunteers confirmed that there was a connection between the p40 values ​​and the brain performance of the participants. According to Prof. Heppner, these results coincide with a US study that showed increased p40 values ​​in the blood serum of Alzheimer's patients.

Clinical studies expected to work as an Alzheimer's drug Although proof of efficacy against Alzheimer's in humans is still pending, theoretically a relatively timely introduction of a drug based on the blockade of p40 would be possible. Because medication to suppress p40 is already used in humans in the context of other diseases, such as psoriasis. "Due to the data and experience on the tolerability of the drug", "a clinical study can now be started without delay," emphasize Prof. Heppner and Prof. Becher. The goal must now be "to bring the new therapeutic approach to the patient quickly." This would be a remarkable success for the researchers, especially since they also patented the use of IL-12 and IL-23 modulators for prevention and treatment of Alzheimer's disease. The clinical studies must now show whether the new treatment approach has also proven itself in humans. (fp)

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