Turning Off Two Immune Proteins Helps Mice with Early-Onset Alzheimer’s DiseaseAn antibody similar to a psoriasis drug reduced amyloid deposits and improved memory as well as cognitive function December 3, 2012 Source: Nature Medicine Summary: A team of researchers, led by senior authors Prof. Heppner and Prof. Becher, found that beta-amyloid deposits in mice engineered to develop a form of early-onset Alzheimer's disease, caused an increase in the levels of two immune protein complexes leading to inflammation and further damage to the brain. Both proteins have a component in common, called p40, so the team delivered p40 antibodies to these mice to neutralize the inflammation caused by these proteins. Post-treatment tests showed that reducing p40 activity led to a 63 percent reduction of beta-amyloid deposits, and improvements in memory and cognitive functions.
Pathological changes typical of Alzheimer's disease were significantly reduced in mice by blockade of an immune system transmitter. A research team from Charité - Universitätsmedizin Berlin and the University of Zurich has just published a new therapeutic approach in fighting Alzheimer's disease in the current issue of Nature Medicine. This approach promises potential for the prevention and treatment of Alzheimer's disease. The accumulation of particular abnormal proteins, including beta amyloid, among others, in patients' brains plays a central role in this disease. Prof. Frank Heppner from the Department of Neuropathology at Charité and his colleague Prof. Burkhard Becher from the Institute for Experimental Immunology at the University of Zurich were able to show that turning off particular cytokines (immune system signal transmitters) reduced the Alzheimer's typical beta amyloid deposits in mice with the disease. As a result, the strongest effects were demonstrated after reducing beta amyloid by approximately 65 percent, when the immune molecule p40 was affected, which is a component of the cytokines interleukin (IL)-12 and -23. Follow-up experiments also relevant for humans showed that substantial improvements in behavioral testing resulted when mice were given the antibody blocking the immune molecule p40. This effect was also achieved when the mice were already showing symptoms of the disease. Based on the current study by Prof. Heppner's and Prof. Becher's team, the level of p40 molecules is higher in Alzheimer's patients' brain fluid, which is in agreement with a recently published study by American colleagues demonstrating increased p40 levels in blood plasma of subjects with Alzheimer's disease, thus showing obvious relevance for human therapy. The significance of the immune system in Alzheimer's research is the focus of current efforts. Prof. Heppner and Prof. Becher suspect that cytokines IL-12 and IL-23 themselves are not causative in the pathology, and that the mechanism of the immune molecule p40 in Alzheimer's requires additional clarification. However, they are convinced that the results of their six-years of research work justify the step toward clinical studies in humans, for which they plan to collaborate with a suitable industrial partner. In the context of other illnesses, such as psoriasis, a medication that suppresses p40 in humans has already been applied. “Based on the safety data in patients,” comment Profs. Heppner and Becher, “clinical studies could now be implemented without delay. Now, the goal is to bring the new therapeutic approach to Alzheimer patients quickly.”
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