New hope in the treatment of Alzheimer's disease
Alzheimer's disease is one of the most common causes of dementia. The main role in the pathogenesis of this disease is played by the accumulation of abnormal versions of proteins in the brain tissue, including beta-amyloid. Researchers from the Charite University of Berlin and the University of Zurich, working under the guidance of Professor Frank Heppner and Professor Burkhard Becher, have demonstrated that the suppression of the activity of certain cytokines (signaling molecules of the immune system) reduces the size of beta-amyloid deposits in a mouse model of Alzheimer's disease. The most pronounced effect – a decrease in amyloid deposits by about 65% – was caused by blocking the activity of the p40 molecule, which is a component of signaling mechanisms mediated by cytokines interleukin-12 and interleukin-23.
Subsequent experiments showed that mice receiving antibodies against p40 showed significant improvement in the results of behavioral tests. Moreover, these effects were observed even in animals that already have pronounced symptoms of the disease.
According to data recently published by the authors and other groups of researchers, patients with Alzheimer's disease are characterized by elevated levels of p40 in cerebrospinal fluid and blood plasma. This fact indicates the importance of the data obtained for the development of methods of treatment of the disease.
The role of the immune system in the mechanisms of development of Alzheimer's disease is currently being actively studied. The authors suspect that cytokines themselves are not causal factors in the development of Alzheimer's disease, and the mechanism of involvement of molecule 40 needs further clarification. However, they believe that the results of their 6-year research work justify the transition to clinical research and are currently searching for a suitable partner from the pharmaceutical industry.
In the context of other diseases, such as psoriasis, drugs that suppress the activity of p40 are already used in clinical practice. Based on the results of studying the safety of such drugs, it can be assumed that the introduction into practice of a new method of treating Alzheimer's disease will not cause great difficulties.
Article by Johannes vom Berg et al. Inhibition of IL-12/IL-23 signaling reduces Alzheimer's disease–like pathology and cognitive decline is published in the journal Nature Medicine.
Evgeniya Ryabtseva
Portal "Eternal youth" http://vechnayamolodost.ru based on the materials of the University of Zurich:
Alzheimer’s Disease in Mice Alleviated Promising Therapeutic Approach for Humans.
27.11.2012