Harmful mutation
Biologists have discovered the first "gene" associated with impotence
Geneticists and molecular biologists have for the first time identified a DNA site in which mutations are associated with an increased likelihood of developing impotence in old age. Its description and other findings of scientists were published in the journal PNAS (Jorgenson et al., Genetic variation in the SIM1 locus is associated with erectile dysfunction).
"The discovery that the vicinity of the SIM1 gene was associated with impotence is extremely important for us because now we can say for sure that this disease has a partially genetic background. This conclusion allows us to look for other "impotence genes" and create drugs that interact with them," said Eric Jorgenson from the Kaiser Permanente consortium in Auckland (in the press release of the First genetic risk factor for erectile dysfunction identified – VM).
As scientists believe today, about every second man aged 40 to 70 suffers from sexual problems, and the probability of their occurrence is rapidly increasing with age. In this regard, according to the ancient Roman and medieval chronicles, little has changed over the past few millennia.
The reasons for the development of impotence, as well as possible methods of combating it, are still the subject of controversy among scientists. All scientific research has so far led only to the creation of viagra, capable of eliminating some of the physical, but not the psychological symptoms of "male" problems, and geneticists have not yet been able to find a single hint of which genes may be associated with their appearance at a relatively early age.
Jorgenson and his colleagues made the first such discovery by analyzing data collected by Kaiser Permanente during genetic testing of approximately 37,000 middle-aged and elderly men living in California.
Some of them suffered from problems with the work of the genitals and took Viagra and some other drugs to combat their consequences. Comparing the differences in the DNA of healthy and sick men, as well as their health and behavior, scientists tried to understand whether there are any segments of the genome that affect the development of impotence.
In total, they were able to identify five single mutations somehow associated with erectile dysfunction, only one of which turned out to be statistically significant. This typo, as scientists note, was not inside a gene, but in a segment of the so-called "junk" DNA, which does not encode proteins, but affects the readability of neighboring genes.
For example, replacing one letter "C" with "T" in this part of the genome led to the fact that the risk of impotence increased by about 25-35% among men of European, African and Latin American origin. Interestingly, the degree of risk increased with age, while such substitutions had almost no effect on the sex life of Asians.
This site, as scientists note, is located in the vicinity of the SIM1 gene associated with the work of the genitals and a tendency to obesity. Scientists suggest that changes in the structure of "junk" DNA may affect the readability of this gene, but the mechanism of their action remains unclear.
The fact is that experiments on cancer cells showed that mutations increased the activity of SIM1, instead of lowering it, as expected by Jorgenson and his colleagues. Further observations, as well as experiments on animals, according to geneticists, will help to find the answer to this question, and to understand which brain cells are responsible for the excitation reaction. This, in turn, will allow the creation of the first full-fledged drugs for impotence.
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