Alzheimer's disease in mice alleviated, promising therapeutic approach for humans 27th November 2012 Pathological changes typical of Alzheimer’s disease have been 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 in the current issue of Nature Medicine. This approach offers potential in prevention, as well as in cases where the disease has already set in. There are now 35.6 million people with dementia worldwide and Alzheimer’s disease is one of the most common causes. Over 7.7 million new cases are reported each year (which implies one new case every four seconds). On current trends, the number of cases will reach 115 million by 2050. The accumulation of particular abnormal proteins, including amyloid-ß (Aβ) 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 amyloid-ß deposits in mice with the disease. The strongest effects were demonstrated after reducing amyloid-ß by 65 percent, when the immune molecule p40 was affected, which is a component of the cytokines interleukin (IL)-12 and -23. Relevant for human therapy 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, 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' research work justify a step toward clinical studies in humans. 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.”
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