The switch of senile diseases
Inflammation is a characteristic manifestation of chronic age-related diseases such as arthritis, gout, Alzheimer's disease and diabetes. However, according to the results of the work of researchers from Yale University, even in the absence of diseases, inflammation can lead to a serious deterioration of various body functions and a decrease in the number of years lived with good health.
The authors, working under the guidance of Professor Vishwa Deep Dixit, have established that the main trigger mechanism of the age–related deterioration of the body associated with inflammation is the activation of the Nlrp3 receptor in the cells of the immune system – macrophages and neutrophils. Activation of Nlrp3 triggers the process of assembly and activation of cytoplasmic protein complexes known as inflamosomes ("inflammation corpuscles"). In turn, the pro-inflammatory signaling cascade triggered by the inflamosomes leads to age-related changes associated with inflammation, manifested by the development of insulin resistance, a decrease in bone density and the extinction of cognitive function.
Dixit and his colleagues studied the process of normal aging of mice that do not suffer from diseases and are kept on a normal diet. Their observations showed that the immune sensor Nlrp3 is activated in response to aging of the body. After that, they demonstrated that a decrease in Nlrp3 activity prevents the development of many age-related diseases in animals, such as dementia, decreased bone density, decreased glucose tolerance, cataracts and thymus degeneration. Such animals were also characterized by better preservation of body functions. They had stronger bones and showed better results when running in a wheel.
The study of another pro-inflammatory receptor activated in response to certain infections and triggering the signaling pathway of another pro-inflammatory protein, caspase-11, did not reveal its involvement in the inflammatory status associated with aging.
In the diagram below from the Yale University press release (there is no other one - try to make out the microscopic letters Nlrp3 and Caspase 11 on it :) on the left is the first of the described signaling pathways of inflammatory reactions, on the right is the second, unrelated to age–related diseases.
According to the authors, further research is needed to study the possibility of manipulating Nlrp3 without compromising the immune system. Dixit also notes that none of the existing anti-inflammatory drugs increases the so-called healthy life expectancy. Therefore, the ultimate goal of the work is to develop therapeutic methods or diets that can suppress the inflammatory process and, accordingly, prevent the development of chronic diseases.
Article by Yun-Hee Youm et al. Canonical Nlrp3 Inflammasome Links Systemic Low-Grade Inflammation to Functional Decline in Aging is published in the journal Cell Metabolism.
Evgeniya Ryabtseva
Portal "Eternal youth" http://vechnayamolodost.ru based on materials from Yale University:
Controlling Triggers of Age-Related Inflammation Could Extend 'Healthspan'.
23.10.2013