Drug stops Alzheimer's in mice

Hope for Alzheimer's Disease - Disease stopped in mice

26/11/2012

The number of Alzheimer's diseases will increase significantly in Germany in the coming decades. Therefore, the search for possible therapies against the hitherto incurable neurodegenerative disease is running at full speed. A research team from the Charité-Universitätsmedizin Berlin, the University of Zurich and the Humboldt University in Berlin has now successfully tested a new treatment approach for Alzheimer's in experiments with mice and the results in the specialist magazine „Nature Medicine“ released.

„By blocking a messenger substance of the immune system, the disease-typical changes could be significantly reduced in Alzheimer's mice“, so the message of the Berlin Charité on the current research results. The new treatment approach promises both in the prevention and in the therapy of the already manifested disease clear successes, 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 scientists around Professor Frank Heppner of the Institute of 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 disease. Over the next 20 years, a doubling of the number of patients worldwide is expected. New treatment approaches for the previously incurable disease are therefore urgently needed. The scientists could now prove, „The fact that switching off certain messenger substances of the immune system, so-called cytokines, which include the interleukins, significantly reduces the amyloid beta deposits in Alzheimer's mice.“ The effect was particularly pronounced in blockade of interleukins 12 and 23 (IL-12; IL23), which both contain the immune molecule p40, the researchers report. Mice that did not have docking sites for p40 or were unable to produce the immune molecule showed a reduction „of amyloid-β by about 65 percent“, so the message of the Berlin Charité.

Improvement of memory in Alzheimer's mice
In subsequent experiments, the researchers found that even in existing Alzheimer's disease, a significant improvement by blocking the immune molecule p40 can be achieved. They injected the animals with blocking antibodies to p40 into the bloodstream or brain. While the injection into the blood remained without significant effect, the mice showed a significant improvement in memory when administering the antibodies to the brain in behavioral tests, the researchers report. Even in people with Alzheimer's disease, the level of the p40 molecule in the brain fluid and in the blood plasma is increased, so that a relevance for the therapy in humans would be obvious. The brain fluid analysis of 39 Alzheimer's patients and 20 healthy volunteers confirmed that there was a correlation between p40 levels and participants' brain performance. According to Prof. Heppner, these results are in line with a US study that has shown elevated p40 levels in the blood serum of Alzheimer's patients.

Clinical trials expected to have effect as an Alzheimer's drug
Although evidence 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 a medication for the suppression of p40 in humans already in the context of other diseases, such as psoriasis, applied. „Based on the data and experience on the tolerability of the drug“, could „now a clinical trial can be approached without delay“, emphasize Prof. Heppner and Prof. Becher. The goal must be now, „bring the new therapeutic approach quickly to the patient.“ This would be a considerable success for the researchers, especially since they also hold the patent for the use of IL-12 and IL-23 modulators for the prevention and treatment of Alzheimer's disease. Whether the new treatment approach also proves itself in humans, must now show the clinical studies. (Fp)

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Picture: Slydgo