A new study has shown that mice bred for Alzheimer’s testing that were given an antibody that blocked the immune molecule p40 showed “substantial” improvements in behavioral testing. The effects were seen even when the mice had already begun showing symptoms of Alzheimer’s disease.

The study was conducted by Dr. Frank Heppner, director for the Institute of Neuropathology at Charité and Dr. Burkhard Becher, professor at the Institute for Experimental Immunology at the University of Zurich. The researchers looked at the accumulation of abnormal proteins, specifically amyloid beta, in the brains of Alzheimer’s patients. The demonstrated that “turning off” specific immune system signal transmitters (cytokines) reduced the amyloid beta deposits in mice with Alzheimer’s disease. The strongest effects came when p40, which is a component of certain cytokines, was affected: amyloid beta deposits were reduced by around 65%.

Based on the results of the new study, the level of p40 in the brain fluid of Alzheimer’s patients is higher. This corroborates a previous study that found increased p40 levels in the blood plasma of Alzheimer’s patients. Though this suggests the study on mice will have relevance for human therapies, the authors of the study emphasized that the mechanism of p40 in Alzheimer’s disease “requires additional clarification. However, the researchers are confident enough that they are currently planning to find an industrial partner to begin the steps toward clinical studies in humans.

“Based on the safety data in patients, clinical studies could now be implemented without delay,” said the study’s authors. “Now, the goal is to bring the new therapeutic approach to Alzheimer patients quickly.”

(Image courtesy UZH)