Authors:
Investigations of this mechanism of aging were conducted by A. Moskalev, F. Wu, S. Imai and other scientists.
History:
Connection between disorders of system regulation and aging was revealed in the neuroendocrine theory of aging. Modern investigations confirm the presence of that correlation.
Example:
Numerous investigations made by Russian and American researches have shown that activation and suppression of certain genes in hypothalamus (a central neuroendocrine t regulator of the metabolism at the base of the brain) can slow down aging in the whole body.
Description:
Regulation of metabolism and homeostasis, as well as realization of system functions (respiration, excretion, digestion, blood circulation, immunity) is very essential. Its disturbance causes varied diseases and increases the probability of death. Simultaneously, all the regulatory processes mentioned above are exposed to
Physiological regulation of all functions of our organism is under control of the nervous and endocrinous systems, and both of them change substantially during aging. Functioning of some brain regions (e.g. hypothalamus, hypophysis, epiphysis) become worse as an organism ages, and this has negative influence at the functions of peripheral endocrine glands (thyroid body, pancreatic gland, adrenal gland, gonads) and diffuse endocrine system. As the result, the level of many essential hormones goes beyond normal and beyond daily rhythmics, and that increases the risk of tens of diseases.
At a cell level, aging is also caused by disorders of regulation. A good half of all the proteins acting in the development of
Additions and Criticism:
Different endocrine glands have different rate of
Publications:
- Satoh, Akiko, and
Shin-ichiro Imai. «Systemic regulation of mammalian ageing and longevity by brain sirtuins." Nature communications 5 (2014). - Matsumoto, A. M., et al. «Aging and the neuroendocrine regulation of reproduction and body weight." Experimental gerontology 35.9 (2000): 1251–1265.
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Imai,
Shin-ichiro , and Jun Yoshino. «The importance of NAMPT/NAD/SIRT1 in the systemic regulation of metabolism and ageing." Diabetes, Obesity and Metabolism 15.s3 (2013): 26–33. -
Wu, Frederick CW, et al. «
Hypothalamic-pituitary-testicular axis disruptions in older men are differentially linked to age and modifiable risk factors: the European Male Aging Study." The Journal of Clinical Endocrinology & Metabolism 93.7 (2008): 2737–2745.
The fact that genetic instability is the mark of aging is supported by the accelerated aging syndrome. It is caused by congenital mutations in genes controlling DNA repair. As the result of those mutations, young people or even children have signs of aging and even look like elderly people. Mutations induced in genes of DNA repair of mice under experimental conditions also result in accelerated aging.
The main functions of our body are under control of genes situated in nuclear chromosomes. Every cell has only two copies of each chromosome, and these copies are not identical — they can have different variants of the same gene (alleles). That is why damages of DNA molecules could badly affect cell functions. The surge of mutations that is observed during aging was called genetic instability. An example of genetic instability is telomere shortening. Telomeres are special areas at chromosome ends. They protect chromosomes so cells with defective telomeres cannot divide and even survive, but sometimes such cells begin to divide in an uncontrolled manner and become tumor ones. When we age chromosomes accumulate damage not only in telomere regions but also along the full length. The main reason of that phenomenon is that mechanisms of DNA repair cease to work effectively. Any damage of nucleotides that form genes or breaks in DNA strands cause mutations in aging cell with repair deficiency. The more mutations cell accumulates, the less viable it becomes and the high risk of its transformation into cancer one arises.
Another reason of genetic instability observed under aging is the activation of mobile genetic elements, also known as «jumping genes» or retrotransposons. Those are 
For preventing telomeres shortening in germ and embryonal stem cells the special enzyme — telomerase — is activated in those cells. Telomerase elongates telomeres after every cell division. In the cells of most human tissues and organs, a gene responding for one of the telomerase components is switched off or works poorly. Accessory effect of that 
Example:
Molecular and cellular mechanisms of stress resistance turning on in the «maintenance mode» can afterwards help to overcome another sorts of stress (e.g. negative effects of radiation). The same mechanisms withstand the 
While the mutation accumulation and the disposable soma theories of aging rest upon permanent pressure of the environmental conditions (predators, diseases), the program of longevity could arise in evolution for overcoming the 
Example:
The concept of phenoptosis signifies the phenomenon of programmed death of an organism.
There are a lot of reasons why cells trigger apoptosis. If a cell finds oneself accidentally in an «alien» tissue or organ, it rapidly «commits suicide». Also, the cell infected with viruses receives a biochemical signal to make 
It should be noticed that evolutionary mechanisms maintaining the program of phenoptosis may be revealed. They are the kin selection (in this case, individuals age and die for the benefit of related members of a group) or the group selection (the death for the benefit of not related individuals). In theory, aging may stabilize the population, increase genetic diversity, and hasten the time of adaptation. Apoptosis in unicellular organisms (like yeasts) and the existence of organisms with «acute» programmed death (like salmon, octopus, and male marsupial mouse) are the arguments in favour of this theory.
Example:
The dual effect of such genes is known as «antagonistic pleiotropy». Antagonistically pleiotropic genes are maintained in populations by natural selection as their early benefits outweigh their late harm.
The antagonistic pleiotropy theory predicts that rapid development of an individual will correlate with rapid aging because the faster puberty is attained — the earlier senescence begins. The theory gives one more prediction: selection towards 
Existence of sexual selection in elderly age. Though the natural selection diminishes in elderly age, the evolution will promote the selection of genes important for the reproduction at an early age in rare cases only. For example, permanently changing, aggressive environment will give advantages to antagonistic pleiotropy. Nevergheless, in actual stable society where there is no abrupt changes and aggressive environment, a tendency exists to have children in later life. In this case, genes promoting healthy longevity and increasing reproductive age will be selected.
History:
In 1961, L. Hayflick discovered that cultured human skin cells have limited capacity to divide — not more than 50 times — after which they become senescent — a phenomenon now known as the «Hayflick limit». However, Hayflick did not explain the mechanisms of this phenomenon.
hypothesis, in each cell division, the end segments of chromosomes — telomeres — are unable to be fully copied. Therefore, telomeres become shorter after each cell division. In a certain moment, telomeres get so short, that cell becomes unable to divide. Such cell gradually lose vital capacity, and this is cell aging properly, according to the telomere theory of aging.
In 1985 an enzyme called telomerase was discovered, and the Olovnikov’s theory was successfully confirmed. Telomerase maintains telomere length in cancer and germ cells, making such cells immortal. As the result, not all the cells have a limit in 50–60 divisions: cancer and germ cells have infinite replicative potential. Nevertheless, relationship of cell aging with telomeres shortening is generally acknowledged.
In some model organisms, such as yeast and Drosophila, there is evidence that reducing oxidative damage can extend lifespan. In mice, interventions that enhance oxidative damage generally shorten lifespan.
If an aggressive, chemically reactive free radical leaves that place where it is necessary, it can damage DNA, as well as RNA, proteins and lipids. Peroxidation is extremely dangerous for polyunsaturated fatty acids that are a component of cell membranes because reaction products (peroxides and hydroperoxides) has also high oxygenating potential. As the result, the process of cell damaging becomes 
The nature provided protection mechanisms from free radicals excess, and most ROS render harmless before they injure any cell structures. The main factors of antioxidant defense of an organism are special enzymes: superoxide dismutase and some other ones. Some antioxidant chemicals are received by the organism with food. Among such antioxidants are vitamin A, vitamin C and vitamin E.
History:
According to this theory, the aging of living organisms depends on casual formation of chemical bonds, or «cross links», between protein molecules. Repair enzymes of the cell can not break those bonds.
The process of cross links formation between protein molecules in a human organism is very similar to the process that takes place during leather tanning. As we age, progressive accumulation of cross links occur in most tissues of our organism — in arteries, cartilages, muscles. The main consequence of this process is the decline in tissue elasticity. Actually, muscle and joint stiffness often observed in elderly people is the result of cross links formation between protein molecules.
The theory was published in 1977. Actually, the disposable soma theory is the particular case of the antagonistic pleiotropy theory of aging.
This theory postulates the existence of genes which control energy resources redistribution from somatic to reproductive cells. These genes properly program the lifespan of a definite species.
This theory receives the support from the observations on populations of wild animals in nature. These observations show that the amount and activity of predators affect the survival strategy of the population predators hunt after. For example, guppies from the population living in conditions of the increased rate of mortality grow faster and breed at earlier age than guppies living under low rate of mortality.
History: 
Gene therapy is still in its infancy. It has the potential to become an important treatment regimen by countering genetic diseases with short life expectancy such as cystic fibrosis. This technology allows to eliminate diseased genes or rescue their normal functions. Furthermore, the transfer procedure of genetic materials allows the addition of new functions to cells such as the production of immune system mediator proteins.
The human embryonic stem cells could be genetically manipulated to introduce the therapeutic gene. This gene may either be active or awaiting later activation once the modified embryonic stem cell has differentiated into the desired cell type.