Abstract
The process of ageing is currently seen as chronic progressive, unstoppable and irreversible changing of the living being's structures and functions, which leads to the decline of its adaptive capacities and increased risk for injuries, diseases and death. The ageing process can be broken down into two closely interwoven components: biological, i.e. normal or physiological ageing, driven by a defined epigenetic/genetic program, and pathological or accelerated ageing, defined by the influence of primarily chronic uncontagious diseases. Presently, a number of theories are trying to answer the crucial questions, how and why this inevitable and complex biological process takes place in all living beings. On one side there are different variations of the programmed ageing theory, and on the other side there are ageing theories based on chronic damage of organism structures and functions that through time lead to irreparable damage, decline of adaptive capacities, weakening of a number of vital functions and in the end inevitable death. It is important to mention the currently actual theories: theory of reactive oxygen species effects (ROS), theory of long protein molecule cross-linking (cross linking theories), mutation theory, autoimune theory, theory of free radical effects (Harman's free radical theory of ageing), non-enzymatic glycation theory of ageing (advanced glycation end product [AGE] compounds), and the above mentioned programmed ageing theory. The most recent experimental research emphasizes epigenetics as the crucial factor in this compound, unstoppable and essentially purposeful process.The close connection between the process of ageing and Alzheimer's disease (AD), and the role of low-density lipoprotein receptor-related protein1 (LRP1) receptor, and the receptor for AGEs (RAGE) in this degenerative disease imply the question of the possible role of these two outstanding multifunctional receptors with numerous ligands in the ageing process. The LRP1 receptor is particularly sensitive to epigenetic factors. Due to abundant methylation, its gene (location 12q13.3), is suppressed with the transcription drop, accompanied by the disorder of its many functions, especially those linked to the drainage of harmful, toxic macromolecules from the brain. The continuing strong DNA methylation of the LRP1 gene promoter progressing during the life cycle, could be the crucial factor in the weakening of numerous processes, all of which have an impact in the accelerated ageing course of living beings. The exceptionally weak methylation of the RAGE promoter, also has a strong impact on the ageing acceleration. This study primarily deals with the essence of the normal biological, i.e. physiological ageing, and tries to avoid as much as possible the impact of the other component, pathological ageing.
