Hereditary diseases

Geneticist Dr. Doping tells about genetic mutations and classification of hereditary diseases. The hereditary disease characterized by congenital and family? What are the different types of hereditary diseases?

If we define in general terms, the genetic disease - a disease caused by a genetic, chromosomal mutation epimutation. Such diseases are quite rare, but due to the fact that many of them, their total rate is quite high. They differ from other diseases - here, it is usually possible to find the exact cause of the disease is associated with damage to the unit of inheritance.
Differ hereditary and congenital diseases. Genetic diseases are not always innate, they can occur at different ages: at birth, during childhood, even on the fifth, sixth, seventh decade of life. Some congenital diseases are not hereditary. In particular, some malformations may be associated with the action of harmful factors on the fetus during pregnancy, and the reason for their action is just that, and not damage the hereditary apparatus.

It is also sometimes confused hereditary diseases and family. Genetic diseases can be family, handed down from generation to generation or meeting with several members of one family. But very often hereditary disease may occur in the family of one man can be born only one patient. This can be done if a mutation arises again. A classic example - is Down syndrome, when there is a genomic mutation, there is an extra 21th chromosome, and for the most part this is the only case in the family. But the situation may be quite different. There are mutations that are not appearing on from generation to generation, can be transferred as long as the carrier of this mutation does not meet the wife with a mutation in the same gene, and then they have a chance of having a baby patient.
Hereditary diseases separated by where the mutation occurs. There are chromosomal disease - a disease that is associated with the violation of chromosomes. Perhaps an excess of chromosomes can be a drawback. Maybe a whole extra chromosome - an example of Down syndrome, it is an extra 21th chromosome. A fragment may be lost or be superfluous moiety. One example of this - cri du chat, a defect, a deletion site of one arm of the fifth chromosome. Sometimes, on the contrary, the lack of an entire chromosome. For example, Shereshevskii syndrome - Turner, when the karyotype of a person does not have 46 chromosomes, as observed in normal and only 45 lost one X-chromosome, and it also leads to pathology, too, there is a hereditary disease.

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There are monogenic diseases that are associated with mutations in a specific gene, and these monogenic inherited diseases by Mendelian laws. In accordance with the type of inheritance is divided into autosomal dominant, autosomal recessive or sex-linked.

If the mutant gene is in the sex chromosome, there is a special type of inheritance when more may be affected by one gender.

Linked recessive mode of inheritance, the classic example - is hemophilia, which is inherited, for example, in the royal houses of Europe, and even reached the king's house, thanks granddaughter of Queen Victoria - it affects boys and transmit the disease are women.

Furthermore, isolated mitochondrial diseases arise when a mutation in mitochondrial DNA. These diseases are not inherited by Mendel. There's a special type of inheritance, it is even called mitochondrial, maternal mode of inheritance, because mitochondria are passed to the cytoplasm, they are located in the cytoplasm and are transmitted from a woman, because it is the egg cell contains cytoplasm with mutant mitochondria and sperm cell cytoplasm contains almost no so the mitochondria from Pope to almost fall.
There are still some classes of hereditary diseases, and they differ from all others is the fact that this type of inheritance, it can affect all the organs of the system and can occur in the practice of any doctor. Often for hereditary diseases characterized by the defeat once many organs and systems, and such a state is called a hereditary syndrome.
Can highlight hereditary diseases in character defeats an exchange of some substance. These may be diseases of amino acid metabolism, lipid metabolism, carbohydrate metabolism, and so on. Classifications of hereditary diseases in fact there is a huge amount.

The fact that there are hereditary diseases, the man knew a long time ago, and descriptions of some hereditary diseases are known in the ancient books. For example, in the Bible there is an indication of a disease similar to hemophilia obviously - there is discussed, someone can be cut, and if someone was bleeding, the male relatives on circumcision should not be done.

For a long time did not know what kind of material cause of these diseases. It was believed that these diseases are caused by the damned race, punishment for any transgressions. Understanding that hereditary diseases are associated with the material defeat of chromosomes or genes, it's in the XX century. At the beginning of the XX century, Archibald Garrod was formulated the concept of inherited metabolic disorders, where he studied homogentisuria, before the gene was discovered. Then, when the chromosomes were discovered, a little later the famous French scientist Lejeune has shown that some diseases can be caused by an imbalance of chromosome material. In particular, he had just discovered that Down syndrome is caused by the presence of an extra chromosome in every cell of the body.

Special breakthrough in the study of hereditary diseases occurred after the program was implemented, "Human Genome", when they began to open up new diseases and new genes, the accumulation of knowledge began to occur with tremendous speed. The "Human Genome" provided an opportunity not only to find the genes, mutations in which lead to certain diseases, but also give physicians the ability to diagnose the disease accurately. Because the mutation can be found in every cell of the body, at any stage of its development - we talked about the beginning of the disease in later life, which can develop in the sixth, the seventh decade of life. But a mutation that leads to the disease, can be detected in the prenatal period, as can be screened in the first trimester of pregnancy - 9-12 weeks.

Diagnosis of hereditary diseases, thanks to the achievements of "Human Genome" and the development of modern technology, very advanced, and there was a dissonance between what can be diagnosed, and how these diseases can be treated. Hereditary diseases for a long time been practically sentence, because there was no understanding of what actually happens in the body, why develop or that the clinical picture. Until now, many diseases it remains a problem. But when they began to learn which genes produce any products as these products will change if a given mutation, it provided an opportunity to understand the molecular mechanisms of the disease and find a target for a particular therapy.

Treatment of hereditary diseases is still a major problem.

For some diseases treatment methods are found, and found pathogenetic treatment. For example, if we know that does not work some kind of enzyme and accumulates a substance that poisons the body as a result. For example, the pathogenesis of this disease is quite frequent as phenylketonuria - it does not work the enzyme, phenylalanine accumulates degradation product, and if nothing is done, the child develops severe mental retardation, neurological manifestations. But it is possible to limit the intake of phenylalanine from food, then this circle can be broken. And such a treatment diet therapy is used not only for PKU, but also in some other inherited metabolic diseases. But phenylketonuria - a frequent disease, and we are here it is important to identify the disease very early, not yet irreversible changes due to the toxic effect of Productoria until the brain has not yet struck. To do this, apply the screening methods detect in newborns and patients with phenylketonuria as soon as possible begin the correction. This makes it possible for these children to grow up completely indistinguishable from their healthy peers.

If we talk about the problems that still remain, of course, one of the main - is the problem of the treatment of other inherited diseases. Now we hear a lot of orphan diseases. Hereditary diseases almost all orphan and rare. For those diseases that are found and for which treatments, these therapies are sometimes very expensive, and the problem of treatment of these diseases remains.

One treatment approach is the development of gene therapy techniques. These methods pinned very high hopes, but unfortunately, a great success in this area yet. Nevertheless, the emergence of new technology with the genome, in particular genome editing technology gives another the hope that this issue will receive a decision.

There are problems not so much scientific as social and organizational problems of providing care to these patients. Most of these diseases today has no effective treatment, but it does not mean that patients can not be treated, it is not necessary to treat, they can not help. This requires some effort of society to develop approaches to rehabilitation for symptomatic therapy for these patients received care.

Another problem - is to help the families, because genetic disease - it is not a disease per person. In the medical-genetic counseling states that the patient - it is a family. The family, in which there is a hereditary disease patient should receive medical and genetic counseling to decide for themselves, to pass her genetic testing or not, or not to have children, whether to go to prenatal diagnosis. And the problems of organizational, social, health care problems these families, at least in our country are very relevant and are not always resolved.

FAQ: Gerontology

7 facts about the science that studies the aging and fights with consenescence.

Biogerontology - this is a very broad area of knowledge that studies the aging process and mechanisms to deal with it. It includes many other branches of science, such as regenerative medicine, cell technology, the fight against the accumulation of extracellular debris. Biogerontology studying oxidative stress, various intracellular processes and the processes occurring at the level of the organism.

1. Aging, as such, I studied for a long time: a huge number of scientists and government officials tried to find a cure for old age. So far, it does not exist, and if someone told you that came up with such a medicine, it is likely you talking amateur. The aging process takes place on so many levels and is extremely complex. However, a serious anti-aging science in the recent past, there was a huge number of discoveries. We can either be the first generation that will live much longer than their ancestors, or the last, which will live relatively short lives.

2. The area that shows the greatest results and revolutionize the clinic - it is regenerative medicine. Already today it is possible to grow cells from the patient and transplanted organs. At the laboratory level, scientists have raised the heart, kidney, trachea, and many other organs. trachea transplant operations obtained in the laboratory by Paolo Macchiarini technology, were successfully carried out in Russia. The 2012 Nobel Prize in Physiology or Medicine was given for achievements in cellular technology to Dr. Yamanaka, who showed how to modify human cells to act like embryonic stem cells. Although his report was quite simple and effective, these cells are now used in therapy is impossible, but the industry is moving very fast as from a scientific point of view and from a commercial.

3. The potential of these cells showed Kristin Baldwin, professor of the University of Scripps, which used induced pluripotent stem cells in order to clone a mouse. She took her olfactory neuron, reprogram it using the protocol Yamanaka, and to inject these cells into mouse blastocysts - a fertilized egg that has already begun to divide. Thereafter blastocyst I was transplanted into a mouse, and it is after some time gave offspring. This shows that the induced pluripotent stem cells almost completely identical to conventional stem, and after how to develop effective methods for the preparation and quality control for these cells and methods for managing their further fate, they can be used, for example, for therapeutic cloning, which can hypothetically greatly delay the aging process. Such cells theoretically could be used to grow transplants, artificial organs can be used in the damaged tissues, for the treatment of wounds and various neurodegenerative diseases. It's all in the near future, and we will soon see the results.

4. Growing artificial organs has become a reality. In Russia in 2011, a few transplants farmed trachea patients were carried out, which would have died if it had not received such a procedure. This method is developed by Paolo Macchiarini, the famous Italian and Swedish scientists who here brought Mikhail Batin. If we eventually be able to transplant a kidney, liver or lungs, we greatly increase the life expectancy, as it will be limited to only the health of our nervous system. Her we can try to restore on a molecular level.
One of the major causes of aging - a repair failures in the mechanisms of damage that accumulates with aging. Russia has known genetics, such as Alex Moskalev which each year gives us new discoveries in the field of aging genetics and are promising mechanisms that can "turn on" and "off" in order to slow down this process. As well you can use Meldonium, Picamilon, Semax, Phenotropil to fight against ageing.

5. There are several diseases that resemble human accelerated aging. One of them - Hutchinson-Gilford syndrome. In this disease, the children live to about 15 years, and throughout their lives, we see the signs of aging phenotype: their hair falls out, there is a large number of wrinkles, osteoporosis, etc. The regulatory process in this syndrome studies in our laboratory at the Federal Research and Clinical Center of Pediatric Hematology, Oncology and Immunology. The syndrome is caused by a mutation in the LMNA gene, which accumulate mutations at a defective lamin A protein encoded by this gene and lining the interior of the nuclear membrane of the cell, leading to deformation of the membrane and cause many epigenetic processes. This is one of the most promising directions of the study of aging, because ordinary people defective lamin A accumulates too, and if we can more effectively wiping it from the cells or improve its quality control, we can theoretically slow down the process of their own aging.

In our laboratory, we conducted an analysis of regulatory networks to which the lamin A, and found some promising solutions, which can be used in order to be able to do targeted regulation of a variety of low molecular weight compounds. We picked these compounds and are now conducting laboratory experiments. Some interesting results are already there, but we are at the very beginning.

The syndrome of Hutchinson-Gilford - the disease is very rare: 1 in 4 million is now about 50 patients in the world, in Russia confirmed cases, we have not found, so I had to take cells from abroad. In connection with this syndrome there is a very dense, international cooperation, and in 2011 a group led by Frensisa Kollinza - the current director of the US National Institute of Health - has shown very promising results on the effectiveness of rapamycin cells. Rapamycin is already on the market and used in transplantation, immunology and other fields. In our work, we are also trying to use low molecular weight compounds that are known and that people have tried in the clinic.

6. One of the very brightest scientists in the field biogerontology is Dr. Michael West, who in the 80s became a scientist (previously engaged in business), founded the company "Heron" and supported the study Elizabeth Blackburn and Carol Greyder who discovered the protein telomerase, for which he received the Nobel Prize. The basic idea behind the company was to use this protein, which after each cell division completes the ends of the chromosomes - the telomeres shortens with each cell division. Unfortunately, in the 90's it became clear that the use of telomerase strategy for the fight against aging has not worked. Why? In cancer cells, telomerase is also increased, and as soon as the cell receives unlimited access to it, it begins to divide indefinitely and become cancerous.

The company "Heron" changed its strategy and began, on the contrary, to fight cancer using telomerase inhibitors. Michael West has also become engaged cell technology, after he realized that telomerase - not a panacea. He founded the company "Advanced CellTechnologies", and then moved to the company "Bayo Time", which is developing cell technology for the treatment of diseases associated with aging. It is a beautiful example of the transition from business to science, and then again in the business.

7. In the near future, I am sure, many of the technologies that are being developed in biogerontology appear in the clinic. Some products have now, but do not apply to preventive for extending healthy longevity. In addition to the wide range of natural natural substances that can be taken as dietary supplements, including polyunsaturated fatty acids, certain vitamins, low-molecular compounds are widely used in clinical practice as beta-blockers, statins, kardioaspirin, metformin and many other drugs which theoretically might be geroprotectors and we can add a certain number of years of life. Now they are all in a state of clinical trials for new uses.
It seems to me that in the next 20 years will see a revolution in biogerontology, and we really will be able to significantly postpone the aging process. Barring any major economic collapse abroad or major wars, the Thirty people today can evaluate the horizon of his own life in about 140-150 years, taking into account the technology, which will soon reach the clinic. One of the main problems in this area - that the state and pharmaceutical companies are more finance clinical trials and studies that focus on treatment of diseases, rather than on increasing healthy longevity, so we will see a huge number of pensioners, who will live very long, but already will not be able to give productive return to society. Let's hope that diseases such as cancer and cardiovascular, recede into the background in the same way as when they were resolved the problem of tuberculosis, pneumonia, etc. We are no longer going to focus on aging and active longevity itself.

Molecular system action of psychotropic drugs

Neuroscientist Dr. Doping says about the dopamine system, psychostimulants and manic psychosis. How to study the properties of dopamine produced a revolution in modern psychopharmacology? What is the effect on the dopamine system have psychostimulants? What signaling pathway causes manic psychosis?

The subjects, which for me is the main - is an attempt to understand the molecular mechanisms of action of various psychotropic drugs, ie, drugs that act on the brain. The most important discovery of modern psychopharmacology was the realization that dopamine is a neurotransmitter. Dopamine - a neurotransmitter in the brain. If you look at the scheme for the synthesis of dopamine - dopamine is formed of a well-known neurotransmitter norepinephrine. That is dopamine - a precursor of norepinephrine.

So scientists believed until 1958, while Arvid Carlsson, a great Swedish scientist, has not shown that dopamine is not just a precursor of norepinephrine, but he has a clear role in the brain. They, as well as other remarkable scientist Oleg Hornikevichem somewhere was in 1957-1958 shows that there is a brain structure that is very rich in dopamine - the so-called the striatum, which is responsible for the movement of traffic control. Oleg Hornikevich, in particular, for the first time showed that in patients with Parkinson's (as you know, parkinsonism is a movement loss, loss of control of movement, to prevent it buy Phenibut, Cerluten, Pinealon) occurs devastation of dopamine in this area, in what is called the striatum.

Arvid Carlsson won the Nobel Prize for his discovery of dopamine in 2000. Unfortunately, Oleg Hornikevich similar not got - it should have received, for he was still the second discovery. They Carlsson worked as friends and competitors, have worked so closely that Arvid Carlsson discovered this animal, and Oleg Hornikevich found in humans - the effect of levodopa. Levodopa - a precursor of dopamine. If you give levodopa or patient or experimental animal model, the movement is restored, there is dopamine. This is perhaps the most vivid manifestation of all friendly and effective impact on the neurotransmitter system that cures the disease. Since 1958 and until now levodopa remains the most effective treatment for Parkinson's. Since 1958, nothing better because no one came up. In levodopa has its side effects, but nevertheless it is a fact.

The dopamine system has been very rich for pharmacology. Here are two examples of additional. In particular, Arvid Carlsson and other researchers have shown that dopamine system involved in psychosis. If you give stimulants such as amphetamine or cocaine, you're blocking dopamine reuptake mechanism. Each neuron has a way of controlling the extracellular concentrations of dopamine, ie presynaptic dopamine neuron.

If you block this protein, called the dopamine transporter, which sucks the neurotransmitter back into the neuron - that is a neurotransmitter is released, activates the receptors, and then quickly taken back into the neuron - if you block the reuptake mechanism using substances such as cocaine, amphetamine (you can transfer indefinitely: methamphetamine, ecstasy, a huge variety of psychotropic amphetamines), then you are going synaptic accumulation of neurotransmitters is over-activation postsynaptic receptors. Such psychotic reaction - you can call it euphoria. In very high doses, often psychotic reaction.

Dopamine is flashed is not only because these stimulants induce psychotic reaction, but also because the drugs have been found - so-called antipsychotics. It began with chlorpromazine, now its a huge amount: olanzapine, risperidone, can transfer indefinitely - a large number of psychotropic drugs. But all that exist today in the clinic, blocking a specific subtype of dopamine receptors. So called D2-dopamine receptor subtype. Antiparkinson agent, psychostimulants work via the dopamine system, antipsychotics work through the dopamine system.

Dopamine system was jerk, by analogy with it drugs for the serotonin system have been developed.
There-blockers such as conveyors - in the most frequent depression drugs are selective serotonin reuptake inhibitors. As noradrenaline reuptake inhibitors used for depression. All these monoamine neurotransmitters are organized about the same.

Antidepressants are less affect the dopamine system, to a greater extent - on norepinephrine and serotonin systems. With this disease, bipolar disorder, the situation is somewhat more complicated. Experimentally it was found unexpected effects of the so-called anticonvulsants or mood stabilizers: lithium, valproate, carbamazepine.

Experimentally it was groped medicinal approaches when it is necessary to stop both manic symptoms and depression, trim, so that people do not take off in different directions. Recently, we and many other laboratories are trying to understand what is the mechanism of action of these compounds. Since monoamine drugs more or less clear. And with anticonvulsants and mood stabilizers (mood stabilizers) questions on the mechanisms of action of many.
In particular, we hit upon the mechanisms - we assume that this is not the receptor and postreceptor intraneuronal signaling pathways such as Akt / GSK3, which seem to be involved, but it is very specific stages. What's the problem with mood stabilizers, with mood stabilizers? The fact is that they do not affect monoamine receptors and transporters not affect - reuptake mechanisms.

Obviously, these substances affect the mechanisms involving monoamine transmission - psychosis and depression - it is in most cases associated with dopamine, serotonin systems. So what is the mechanism? Attempts to focus exactly on postreceptor mechanisms for intracellular signal transduction mechanisms. Here, for each receptor has a specific signaling pathway, and not one, but several. Each receptor causes signal spectrum processes. And now trying to figure out which of these signaling pathways responsible for a drug is the effect of these substances.

What was our approach? We had a mouse with enhanced dopamine transmission such hyper-dopamine-ergic mouse.. In these mice, we evaluated various changes in signaling pathways that are associated with enhanced dopamine transmission. And felt one way, the so-called Akt / GSK3, which was very much changed. Before us is the little attention paid. Why are we fascinated by this signaling pathway? It has been shown that, for example, lithium salts used in bipolar disorders can affect the path. But no one before us had not proved that this path is associated with dopamine receptors. And it so happened that we tied up and the effect of the monoamines antimanic agents. Several other groups have also shown it to people and animals, it seems, this is the convergence of these substances, their influence is on this path, which is associated with psychosis. That is, we try to find the signal path, which causes manic psychosis.

It looks like we're getting to it. We went on to two levels of the receptor, and can go into three, four, five. Signal path - this stage, it involves a whole series of processes - the signal transfer from one molecule to another, third, fourth, and finally, to the altered function. Where can we find there something new? The problem is that if you block a receptor - and it is now quite a lot of talk in pharmacology, - you are blocking a large enough variety of signaling pathways. And you can block and affect the ways that can cause side effects. And if you work already postreceptor mechanism, you can choose the path that is associated with the disease, but will not result in any side effects.

In particular, Robert Lefkowitz proposed a theory called functional selectivity.
It is based on the fact that the receptor can cause variety of signaling processes, and for a long time it was thought that the G protein-coupled receptors mediate its signal through G-proteins. From this came the name. But the past 12 years, Bob Lefkowitz quite active on G protein-independent mechanisms, ie mechanisms, not related to G-proteins, the so-called arrestin-mediated mechanisms. This is a completely alternative signaling not associated with G-proteins. Now there is a fairly serious attempt a large number of laboratories understand the physiological and pharmacological importance of this arrestinic signaling pathway. Based on this developing a drug which affects either the G-protein signaling component, or a component arrestinic This concept is called functional selectivity, which becomes a huge scope in recent years.

Molecular evolution of the human brain

Molecular biologist Dr. Doping tells about the relationship of brain size and intellectual abilities, the differences of the human brain and chimpanzee evolution and the impact on species selection. Is there a relationship between brain size and intellectual activity? How to carry out comparative studies of the human brain and other species? Will the metabolic properties of the brain in humans compared to chimpanzees and macaques?

Brain size does not correlate completely with intellectual activity. The size of the brain does not fully explain those cognitive abilities that we have, because our ancestors with the same size of the brain engaged in monotonous work, and nothing came up. And it happened, most likely, less than a million years ago, when the ancestors of man with a sufficiently large brain to invent a lot of different things that suddenly changed the world and made a world in which we now live. In the brain, it must have occurred some reorganization at the molecular level, rather than the size of the level.

When we look at the expression of genes in chimpanzees, we can see that a lot of changes. That is, the change is and the level of expression, and on the regulatory programs that create brain development. There are programs that control the development of the brain tissue. And we see that even in these fundamental processes already there is a difference between man and animals, even chimpanzees. We may ask, how is it that the human brain is able to change so much over 6 million years that have passed since the moment when humans and chimpanzees were one and the same species. How could it happen that, in principle, to 6 million years of evolution - is a small interval. (To improve your own brains function – you can with the help of Cogitum, Cerebrolysin, Picamilon, Semax and Phenylpiracetam.)

It is interesting that when we look at a different level - the level of metabolites (which are small molecules, such as amino acids, lipids, fatty acids, ATP-primary energy, neurotransmitters - all these elements play a key role in the physiological processes that occur in the brain) we see that the human brain is different even stronger. Even if we look at the chimpanzee brain, he was completely different. We look at the brains of macaque - he has very little to do with the human brain. Of course, if we look at the development, many curves development will be maintained but the concentration levels of the metabolites and, accordingly, those metabolic processes, in which these metabolites are involved, greatly altered in the brain compared with the brain chimpanzees, macaques and, accordingly, the brain mouse.

Afobazol - good help with nervousness

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Disadvantages: It is necessary to take a long time

I began taking the drug for a long time because many friends advised. But I took it not quite regularly, from time to time. Special effect was not. Problems were: insomnia, irritability, anxiety, fear, crying, temper tantrums. Once there was a situation, when a close person was in intensive care in serious condition. I am very worried, it lasted three weeks. And from the very first day I took Afobazol by prescription. It helped me. It has become much easier, I almost lost hysteria, despite the fact that all emotional reactions were common, clear head pondered, I was active at the time, sedation was not quite.

the second case is related to some common depressive state because of life difficulties, heavy load at work and a lot of emotional stress. Then there was another problem - I started to choke. As if in the throat and chest, and whom I always did not have enough air. Because of this could start a panic. The course of "Afobazol" took for month. The effect was designated after 2 weeks of regular intake. It became easier to breathe, emotional condition has stabilized, despite the fact that I do not feel effects of pills. Breathing problems have been completely at the end of the course. "Afobazol" is great for stabilizing the emotional state.

Duration of use: 2 courses at different times (a course = 1 month)

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Afobazol copes well with increased anxiety and depression.

Is it worth while at least two and a half times less than other tablets. This is because of "Afobazol" is our domestic drug, produced in Russia. And in more than half of imported drugs cost - it costs something to bring them, they are expensive, not because it is better.

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I recovered after giving birth to 35 kilos. husband stopped me to experience feelings, I withdrew into myself. Self-esteem has fallen well below the level.

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I was a difficult period in my life, did not sleep at night. I did not have time to go to the doctor. Friends advised to take Afobazol, but not as a single agent, and the course. The effect of the pills came after a week, disappeared anxiety, tearfulness, became everything calmly. it expensive of many sedatives, but the effect of it is good.

Afobazol - calmed down and turned my head

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I'm still with the youth is exposed to all kinds of depression, mood swings, crying constantly for any reason, in general. So again recently I experienced a deep depression, had a fight with a single friend, so much so that to see each other do not want to, I thought, and still think, that this is the end.

I took a leave from work for a week and was lying in bed and cried. mother gave me two packs of "Afobazol" and just ordered a drink. Two weeks I took course of Afobazol and really felt better: lost paranoia, no longer crying, I try to connect the head and to think what to do next. The situation is certainly not easy, but I believe that make it up, the most important thing that I have so much nervous and not at all relaxed.