The ageing of the body consists of a series of interconnected processes. Recent biomedical research has led to the development of the “hallmarks of ageing”, the processes that control the ageing process at cellular level.
Epigenetic changes
Our genome consists of long strands of DNA wrapped around protein coils (histones). These histones are equipped with chemical devices that support the switching on and off of genes. These switching devices form the so-called epigenome. The epigenome changes with age, which can impair the smooth coordination of gene activity. Sirtuins are a particularly well-studied group of enzymes that influence the epigenome. However, diet, medication or lifestyle modifications can also alter the epigenome.
Loss of proteostasis
The main task of genes is to produce proteins. These regulate practically all chemical reactions in the cell and must be folded into precise shapes in order to fulfill their task. In old age, misfolding occurs due to epigenetic damage, as a result of which the proteins no longer fulfill their task. The process that regulates the maintenance of all proteins in their original form is called proteostasis.
Deactivated autophagy
Autophagy is a process in our cells that breaks down damaged or non-functioning cell components and reuses their components. It is a kind of recycling mechanism. This function is essential for maintaining cellular health and protecting against toxic build-up. Autophagy decreases with age, which means that cellular “waste” such as damaged proteins or organelles are no longer completely removed. This promotes the development of age-related diseases such as neurodegenerative diseases or cancer.
Deregulated nutrient measurement
If there are plenty of nutrients in the body, the cells multiply. However, if they are scarce, the body concentrates on maintenance and repair. Studies have been developed to simulate nutrient deficiencies in the body by means of food reduction and/or medication. These strategies have improved health and longevity in animal studies.
Dysfunction of the mitochondria
Mitochondria are the “powerhouses of the cell”, but they also produce free radicals (reactive oxygen species or ROS) that damage cells. A new line of thought suggests that oxygen radicals may be important in signaling cellular stress, causing cells, organs and tissues to increase their maintenance and repair processes. See also
Cellular senescence
Cellular senescence is a phenomenon in which cells stop dividing. With increasing age, these ageing cells accumulate and release harmful signals into the environment. The cause of cellular senescence is a shortening of the telomeres, DNA components in the chromosomes that are important for all biological processes. They are associated with ageing.
Recent work in which mice were genetically engineered so that researchers could eliminate many of their senescent cells has shown evidence of health benefits, including a longer lifespan. Work is currently underway to identify drugs that target the elimination of senescent cells.
Depletion of stem cells
Our body’s ability to regenerate tissues and organs depends on healthy stem cells. They can differentiate into different cell types and then replicate as required. With increasing age, the stem cell pools are depleted or the ageing stem cells no longer function as well.
Altered intracellular communication
Communication between cells and tissue is essential for maintaining bodily functions. Hormones, for example, are important messengers for cell communication. Age-related chronic inflammation, presumably as a result of senescent cells, can significantly reduce or disrupt communication. Restoring proper intracellular communication could improve health, e.g. by reducing chronic age-related inflammation.
Chronic inflammation
Chronic inflammation is another feature of ageing that is characterized by persistent inflammatory responses throughout the body. In contrast to acute inflammation, which provides a rapid and effective defense against threats such as infections, chronic inflammation remains active over a long period of time. It is often triggered by age-related factors such as senescent cells, damaged DNA or dysfunctional mitochondria. These inflammatory processes can lead to a deterioration in cell and tissue function and increase the risk of age-related diseases such as Alzheimer’s, diabetes and cardiovascular disease.
Dysbiosis of the microbiome
The microbiome, which is found in the human gut, plays a particularly important role in our health and the ageing process. The older we get, the more the composition of our intestinal flora changes. This process is known as dysbiosis. The change can weaken the immune system, promote chronic inflammation and impair the absorption of nutrients. Dysbiosis is also associated with age-related diseases such as diabetes, heart disease and neurodegenerative disorders.
Genomic instability
The genome, or the genetic material of a living organism, is responsible for the smooth running of all bodily functions. External or internal pollutants, such as pollution or free radicals, constantly damage the DNA in our cells; cellular repair processes can recognize and compensate for this damage. With increasing age, the damage to the genome accumulates and the repair processes can no longer keep pace. Cancer is a consequence of unrepaired DNA damage. Living organisms with impaired DNA repair processes show signs of accelerated ageing.
Telomere shortening
Telomere attrition is a particular type of genomic instability. Telomeres are repetitive DNA sequences that protect the ends of chromosomes and prevent them from being confused with broken strands of DNA. Telomeres determine our lifespan and are shortened by normal cell division, but also by processes that damage the DNA. When telomeres reach a critically short length, cell replication is switched off. Telomerase, an enzyme of the cell nucleus, can prevent the shortening of telomeres and even restore telomere length.
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