Interleukin-33 against Alzheimer's disease
Researchers working under the leadership of Professor Eddy Liew from the University of Glasgow and Professor Nancy Ip from the University of Science and Technology of Hong Kong have demonstrated that the protein interleukin-33 (IL-33) eliminates the manifestations of simulated Alzheimer's disease and cognitive decline in mice.
Alzheimer's disease is a serious age–related disease that currently has no effective treatment. It is the most common cause of dementia (dementia) and affects about 850,000 people in the UK alone, mostly aged 65 and over. This disease affects approximately every fourteenth person from this age group, while the frequency of its occurrence is inexorably increasing simultaneously with the increase in the population of elderly people. According to statistical forecasts, by 2030 there will be about 65 million people with Alzheimer's disease in the world.
As a model of this disease, the authors used a line of APP/PS1 mice, which develop a condition similar to Alzheimer's disease as they age. These animals have all the typical manifestations of this disease, including the accumulation of extracellular amyloid plaques and neurofibrillary cords in the brain tissue. As the disease progresses, the number of plaques and strands increases, which leads to violations of interneuronal contacts and, ultimately, to the death of nerve cells and a decrease in the volume of certain regions of nervous tissue.
Interleukin-33 is a protein produced by cells of various types. Its highest concentrations are characteristic of the central nervous system (brain and spinal cord). The authors demonstrated that the administration of interleukin-33 to aging mice of the APP/PS1 line within a week restores their memory and cognitive function to levels characteristic of normal animals.
Apparently, interleukin-33 acts by mobilizing microglial cells (immune cells of the brain) that surround amyloid plaques, destroy and digest them, thus reducing the number of protein aggregates in brain tissue. This is due to the induction of the synthesis of the enzyme neprilysin, which degrades soluble amyloid.
In addition, interleukin-33 therapy provided inhibition of inflammation in brain tissue, which, as earlier studies have shown, contributes to the formation of toxic plaques and aggregates. Thus, interleukin-33 not only helps to eliminate already formed plaques, but also, first of all, prevents the formation of new protein deposits.
At the same time, Professor Lew notes that today it is unclear whether the described approach is applicable to human Alzheimer's disease. However, there are good prerequisites for this. For example, earlier genetic studies have demonstrated the existence of an association between mutations of the gene encoding interleukin-33 and the development of Alzheimer's disease in European and Chinese populations. Moreover, it is known that the concentration of interleukin-33 in the brain of patients with Alzheimer's disease is lower than in the brain of healthy people. Currently, the authors are on the verge of starting a phase I clinical trial, the purpose of which will be to test the toxicity of interleukin-33 in dosages corresponding to those used in the study.
The article by Amy K. Y. Fu et al. IL-33 ameliorates Alzheimer's disease-like pathology and cognitive decline is published in the journal Proceedings of the National Academy of Sciences USA.
Evgeniya Ryabtseva
Portal "Eternal youth" http://vechnayamolodost.ru based on the materials of the University of Glasgow: Protein research offers "promising" potential treatment of Alzheimer's disease.
25.04.2016