An important gene for life span is discovered, will old age be treated?

Scientists who have conducted new research to find out what mechanisms lie behind this effect believe that new discoveries should allow the development of antiaging drugs.

Research into the aging process and its slowdown has become increasingly popular in recent years, as it may become the basis for a lucrative industry against aging.

For example, research has shown that metformin, one of the diabetes drugs, extends the life span of people with diabetes, although they would be expected to live a little shorter. This drug is said to be very popular among Silicon Valley's billionaires.

One of the objectives of aging scientists is, among other things, find Sirt6.

Numerous studies have previously confirmed that the activities of this gene, which can be found in humans but even in many animals, are important in cellular functions and diseases, in restoring DNA, and are closely linked to life expectancy.

In a new study, Vera Gorbunova of Rochester University in New York, and her colleagues decided to find mechanisms that affect life expectancy because that meaning is the key to eventual development of substances that can have an effect on aging.

Research into molecular function and the role of Sirt6 in aging and life expectancy in Drosophila fruit flies have shown that the extensive expression (Overexpression - Sirt6's OE under experimental conditions affects life expectancy in low-cellular eucariotic organisms as well as in many higher organisms. It also found that a key mechanism with which the extensive expression of dSirt6 causes life expectancy to be extended is to suppress the activity of demyc transliterated, a protein associated with the formation of multiple tumors in humans.

The authors stress that one of the most exciting discoveries is that increasing the level of expression of the figure -- Sirt6 -- extends the life span of mice.

In addition, authors indicated that the expression Sirt6, improved by the geneSwit inclusion system. ch - GAL4, enough to extend life expectancy, can start at adulthood and not exclusively during early stages of development. This means that possible drugs can affect longevity even if the body is not programmed to increase the expression of Sirt6 in an early stage of development. Specifically, in all available research, scientists have genetically modified animals so that they essentially have increased Sirt06's expression, then no therapy was given.

The authors write that some recent research has already revealed that Sirt6's extensive expression using the GeneSwitch system extends the lives of mice, beavers, and fruit flies, which supports the the thesis that Sirt6 is quite specific to use to prolong life.

Furthermore, scientists found that OE dsirt6 specific for fat tissue is sufficient to prolong life, and it is known that the fat tissue of the fruit fly is an analog of fat tissue, liver, and an immune tissue of mammals.

It is also interesting to note that in mice stretched from the growth of Sirt6 in the liver and white fat tissue, the ACT's lower phsphalization, which plays a key role in numerous cellular processes such as metabolicism and proliferating glucose, migration, and programmed cell death, was observed.

A recent study also found that increasing Sirt6's expression protects from aging related to reducing the production of hepatitis and homeostase. Together, these findings suggest the importance of these tissue in extending life expectancy using Sirt6.

Understanding Sirt6 Action Mechanism

The main purpose of the new study, the authors write, was to understand better the molecular mechanisms with which dsirt6 extends life expectancy. The analysis showed that dSirt6 is a powerful negative regulator of the genes of ribosome biogens and protein synthesis, which are also the intended genes for dMyc.

But the study showed that OE dSirt6 doesn't work to prolong life just by reducing the dmyc activity.

The team believes that a possible explanation is that increasing the expression of dsirt6 in fruit flies improves the repair of DNA defects and reduces the RTE expression, which are two additional functions of Sirt6 that are strongly linked to aging and longevity.

This survey is in line with previous findings that SIR6 improves the repair of two-line DNA fractures, one of the kinds of damage to our genetic material.

The authors write that in recent years small molecules of the Syrt6 gene activators have been identified, which opens up the possibility that their use can increase the activity of this enzyme, and these compounds can be used to prolong human health and to treat aging diseases.

Why Sirt6?

Sirt6 is not the only gene that participates in DNA repair. However, the director of the new research, Vera Gorbunova, thinks he's more interesting than others from therapeutic point of view, because DNA repair seems to be his primary function.

For example, the FOXO3 gene is also involved in DNA repair, but being responsible for several other functions in the cell, increasing its function would have impact on several other important mechanisms in the cell. This makes Sirt6 one of the potential objectives of developing new anti-aging therapies.

But it should be noted that the trip from laboratory to medicine is usually very long.