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Analogues of Nootropil

Level 4 ATX code matches:
Bravinton

Acefen

Carnicetine

Pyracesin

Nooclerin

Semax

Piracetam

Olatropil

Fezam

Vinpocetine

Cerebrocurin

Cavinton Forte

Calcium hopantenate

Glutamic acid

Cephabol

Olanzapine

Cerebrolysate

Pramistar

Sidnocarb

Vinpotropil

Analogues are the following drugs: Biotropil , Lucetam , Piracetam .

The price of Nootropil analogues is lower and higher. For example, Piracetam costs less.

Which is better: Nootropil or Piracetam?

The medicines are generics, that is, they contain one active substance, piracetam, and have a similar effect on the body. The drug Piracetam is domestically produced and therefore costs less, however, it is also considered less purified.

Application of Biotredin in the practice of a neurologist

Purpose of the review: to provide information about the possibility of using the drug Biotredin in the practice of a neurologist.

Basic provisions. Deficiency of pyridoxine (vitamin B6) is associated with such neurological diseases as pyridoxine-dependent epilepsy, attention deficit disorder (hyperactivity disorder), cerebrovascular disorders due to hyperhomocysteinemia, etc. Data are provided on the effectiveness of correction of metabolic disorders by exogenous administration of B vitamins. Information on the use of domestically produced vitamins is reviewed. the drug Biotredin for certain diseases of the nervous system. The authors provide recommendations for the use of this drug in clinical practice.

Conclusion. Biotredin is a promising drug, the use of which is advisable in patients with various diseases of the central nervous system.

Key words: pyridoxine, threonine, epilepsy, stroke, treatment, Biotredin.

The state of the nervous system largely depends on the timely entry into the body of not only energetic oxidation substrates, but also a number of substances that are directly involved in numerous complex biochemical processes that ensure the normal functioning of neurons and glial cells. For the correct functioning of enzyme systems, aimed at preserving the structural integrity of the cell itself and its organelles, producing a sufficient amount of neurotransmitters and maintaining the activity of synapses, a sufficient concentration of vitamins, amino acids, proteins and other nutrients is needed in the brain tissue.

These biologically active substances take part in the most complex processes of the formation, maturation and functioning of nervous tissue, in the implementation of neuroplasticity processes, the acquisition of new skills and compensation for impaired functions [2]. Their lack in the body, impaired absorption in the gastrointestinal tract, genetically determined disorders of their synthesis or utilization can lead to severe structural and functional changes in the nervous system [16]. However, drug or dietary correction of this type of disorder, restoration or compensation of functions impaired due to the disease are possible.

The normal functioning of the nervous system is ensured by amino acids and vitamins. Most of them are not synthesized in the body and must come from outside [7]. One of these essential amino acids is threonine. Threonine is closely related to protein metabolism in the body; it is involved in the formation of muscle tissue proteins and in maintaining adequate protein balance. In addition, threonine has a positive effect on the liver, cardiovascular and immune systems. Due to its active participation in protein synthesis, it helps strengthen bone tissue. One of its important metabolic effects is its participation in the catabolism of fats and fatty acids and their inclusion in subsequent metabolic processes.

Entering the cell, threonine is included in the formation of the amino acids glycine and serine, which are also involved in protein synthesis, improving the structure of muscle tissue, including the myocardium. Threonine is a necessary component in the synthesis of collagen, elastin, and various antibodies. It is believed to have the ability to reduce intolerance to gluten found in wheat grains.

In the formation and functioning of the human brain, serine-threonine kinase plays an exceptional role, which ensures the perception of many influences on the neuron and the transformation of external signals into stimuli that ensure the processes of development of nervous tissue and neurodegeneration [19]. Threonine is of great importance in the functioning of a number of neurotransmitter systems, in particular glutamate receptors, in the central nervous system [17]. It has been established that calmodulin-dependent protein kinase 11 interacts with the metabotropic glutamate receptor under conditions of phosphorylation of threonine [12]. There is also data suggesting a close connection between serine-threonine kinase and the implementation of the activities of other neurotransmitters important for the functioning of the brain - cannabinoids, serotonin, μ-opioids [6, 16].

It is believed that it is thanks to serine-threonine kinase that a wide range of growth factors such as insulin-like, brain-derived neurotrophic factor and some others influence nervous tissue [21]. Due to its metabolic effects, threonine indirectly (through the synthesis of a number of compounds involved in the functioning of the central nervous system, in particular in the regulation of the exchange of nerve impulses between neurons) affects the processes of memory consolidation and information assimilation. It also has an antidepressant effect.

A significant portion of threonine is metabolized immediately after entering the body. Thus, when applied sublingually, threonine and vitamin B6 are quickly absorbed and enter the neurons of the brain. With the assistance of pyridoxine hydrochloride, threonine participates in a sequence of chemical reactions that results in the formation of the amino acid glycine. Replenishment of the glycine pool in the brain enhances the processes of active internal inhibition without suppressing the functional activity of neurons.

Due to the diverse metabolic effects of B vitamins, including those realized in the tissue of the central and peripheral nervous system, their preparations are widely used in clinical practice. The results of experimental and clinical studies indicate their important role in various biochemical reactions in neurons and glial cells. Pyridoxine (vitamin B6) as a coenzyme is involved in the reactions of decarboxylation and transamination of amino acids in various tissues, including the peripheral nervous system [9].

Numerous studies indicate that B vitamins, in particular pyridoxine, are involved in a variety of metabolic processes occurring in nervous tissue. In many cases, their introduction into the body helps normalize metabolism and has a stimulating effect on the course of reparative processes in nervous tissue under conditions of damage, for example, it helps restore impulse transmission along damaged nerve fibers [5, 11]. In clinical settings, the effectiveness of pyridoxine has been demonstrated in patients with various forms of damage to the peripheral nervous system (polyneuropathies of various origins, spondylogenic dorsopathies, discogenic radiculopathies).

In recent years, information has been obtained that a deficiency of pyridoxine in the body and disorders of its metabolism of various origins are associated not only with damage to the peripheral nervous system, but also with some diseases of the brain. Thus, the results of a number of studies provide strong reasons to believe that pyridoxine deficiency may be one of the causes of attention deficit hyperactivity disorder [8].

This assumption has received clinical confirmation: according to the results of the study, the daily urinary excretion of pyridoxine metabolic products is closely related to the metabolism of monoamines. This seems extremely important, since, according to modern views, it is disorders of adrenergic neurotransmission that underlie the formation of attention deficit hyperactivity disorder [14]. Moreover, evidence has been obtained that long-term (over several years) systematic use of pyridoxine helps mitigate the course of the disease.

Similar information is available regarding pyridoxine-dependent epilepsy [13, 15]. It has been demonstrated that the metabolic characteristics of individual people lead to an increased sensitivity of the body to pyridoxine deficiency and this can manifest itself in repeated epileptic seizures.

Similarly, the complex and varied metabolic consequences of pyridoxine deficiency in the body due to disruption of adequate synthesis of neurotransmitters, changes in the sensitivity of receptors to them, etc. can lead to cognitive impairment [18]. Violations of vitamin metabolism can cause progressive cognitive disorders both due to increasing vascular damage to the brain and through the mechanism of accumulation of β-amyloid in brain tissue [10]. It has been established that systematic administration of pyridoxine into the body slows down the accumulation of β-amyloid in neurons.

Considering the largely synergistic effect of pyridoxine and threonine on brain tissue and their joint participation in a wide range of metabolic processes, simultaneous use seems quite justified. It is also important that the metabolic processes of these substances are closely interconnected, as evidenced by the results of experimental studies [20]. There is evidence that threonine, in the presence of pyridoxine (vitamin B6), breaks down into the amino acid glycine and acetaldehyde, stimulating inhibition processes and redox reactions, respiration processes and ATP synthesis. This fact confirms the feasibility of their joint use.

Currently, the drug Biotredin is registered in the Russian Federation. The drug contains 100 mg of threonine and 5 mg of vitamin B6. Available in the form of tablets for sublingual use. Threonine, with the participation of pyridoxine, breaks down into the amino acid glycine and acetaldehyde (AcA). Further transformations of AcA and glycine occur independently. An important aspect of AcA metabolism is its conversion to Acetyl-CoA, which is a substrate of the tricarboxylic acid cycle. Thus, an increase in the concentration of AcA promotes the activation of the Krebs cycle and the formation of ATP. Glycine, in turn, activates the mitochondrial respiratory chain, improves cell bioenergetics and, together with AsA, participates in many metabolic processes.

Sublingual use of a combination of threonine and pyridoxine provides a quick and effective effect on the central nervous system. The property of Biotredin to increase the processes of active internal inhibition and at the same time the functional activity of cells determines the pharmacological effects of the drug:

• increased concentration and increased mental performance;

• strengthening the volitional message to complete the task;

• reduction of psycho-emotional stress, improvement of mood;

• improvement of short-term and long-term memory;

• reduction of pathological craving for alcohol and substance abuse phenomena.

In chronic alcoholism, due to the excess intake of ethanol in the body, an excess amount of AsA is formed, which is constantly maintained at a certain level due to frequent alcohol consumption. The body stops producing AsA, and if you do not drink alcohol, a kind of withdrawal occurs, because normally AsA is constantly present in the blood in an amount of 0.19 nmol. The absence of endogenous AsA explains the hangover syndrome (headache, feeling of exhaustion throughout the body, etc., when you don’t want to live). Biotredin compensates for this lack of AsA, and the hangover syndrome is not so severe. Therefore, Biotredin is prescribed to people who abuse alcohol; when actualizing a pathological craving for alcohol, especially combined with affective (irritability, low mood, internal discomfort), sensory (feelings of hunger) and ideational (“thoughts about alcohol”) disorders; with withdrawal syndrome caused by sudden withdrawal of alcohol consumption; to maintain remission in patients who have stopped using it [1].

At the same time, the possibilities of using the metabolic effects of the drug in other diseases of the central nervous system are being studied. Thus, a study was conducted on the use of Biotredin in combination with Limontar (citric acid + succinic acid) and glycine in patients with acute ischemic stroke [3]. Its results indicate that complex therapy with these drugs in combination with basic treatment leads to an increase in the number of surviving patients and a decrease in the severity of focal neurological deficit. The authors noted that motor functions are restored first, and a positive effect is observed even in patients hospitalized in serious condition. The increase in motor activity relative to the initial level was statistically significant.

It is noted that the positive effect of combination therapy is observed not only in adults, but also in children. Thus, the use of a complex of metabolic drugs, including Biotredin, facilitated the experience of cerebral ischemia and hypoxia in newborns [4]. As they grew older, the children did not lag behind their peers in their development, despite suffering brain damage. The differences from children from the control group who did not receive combination treatment were statistically significant.

Taking into account that a deficiency of pyridoxine in the body can be associated with a number of neurological diseases, the possibility of using Biotredin in patients with pyridoxine-dependent epilepsy, a number of cognitive disorders as part of neurodegenerative diseases, etc. is of undoubted interest. It is possible to prescribe Biotredin to patients with homocysteinemia in order to prevent acute ischemic stroke and chronic cerebrovascular accidents.

As clinical practice shows, Biotredin is well tolerated by patients. Registered side effects include rare dizziness, increased sweating, allergic reactions (vitamin B6 intolerance).

Contraindications to the use of Biotredin are alcohol intoxication, simultaneous use of medications that inhibit the functional activity of the central nervous system (anxiolytics, antipsychotics, antidepressants, hypnotics, etc.), as well as hypersensitivity to vitamin B6. The use of the drug is not contraindicated for pregnant and breastfeeding women.

Biotredin is produced in the form of sublingual lozenges. They can be crushed before use. Dosage regimen: 1 tablet 2-3 times a day for 3-10 days. If necessary, the course is repeated 3-4 times a year or more. Patients who abuse alcohol are prescribed 1-3 tablets 2-3 times a day for 4-5 days. If necessary, the course is repeated 5–10 times a year. In case of relief of alcohol withdrawal syndrome: on the first day - 1-4 tablets 3-4 times (daily dose - 3-16 tablets); on the second day and beyond - 1-2 tablets 2-3 times a day (daily dose - 3-6 tablets) for 21-28 days. The course can be shortened to 10–14 days.

During the period of remission, to identify a hidden craving for alcohol, take 2-3 tablets of Biotredin on an empty stomach. The appearance of mild dizziness, a calming effect, facial flushing, and sweating within 10–20 minutes indicates the presence of a hidden craving for alcohol. In this case, a 5–10-day course of Biotredin is recommended: 1–2 tablets 2–3 times a day along with glycine (100 mg sublingually 10–15 minutes before taking Biotredin) [1].

Conclusion

The presented data allow us to consider Biotredin as a drug with significant prospects for use in a variety of diseases of the central nervous system.

LITERATURE

1. State register of medicines. Biotredin. URL: https://grls.rosminzdrav.ru/

2. Gusev E.I., Kamchatnov P.R. Plasticity of the brain in normal and pathological conditions // Zhurn. neurology and psychiatry named after. S. S. Korsakova. 2004. T. 104. No. 2. P. 73–80.

3. Gusev E. I., Komissarova I. A., Alferova V. V., Nartsisov Ya. R. Experience of using the metabolite complex of drugs Glycine, Biotredin, Limontar in the treatment of ischemic stroke // Terra Medica. 2001. No. 4. P. 37–38.

4. Dzhumagaziev A. A., Belopasov V. V., Rakhimova L. R. The use of metabolites in children with perinatal hypoxic-ischemic lesions of the central nervous system // VII Russian National Congress “Man and Medicine”. M., 2000. P. 346.

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7. Cooper J. Nutrition and the brain: what advice should we give? // Neurobiol. Aging. 2014. Vol. 35. Suppl. 2. P. S79–83.

8. Dolina S., Margalit D., Malitsky S., Rabinkov A. Attention-deficit hyperactivity disorder (ADHD) as a pyridoxine-dependent condition: urinary diagnostic biomarkers // Med. Hypotheses. 2014. Vol. 82. N 1. P. 111–116.

9. Hankey G., Ford A., Yi Q., Eikelboom JW et al. Effect of B vitamins and lowering homocysteine on cognitive impairment in patients with previous stroke or transient ischemic attack: a prespecified secondary analysis of a randomized, placebo-controlled trial and meta-analysis // Stroke. 2013. Vol. 44. N 8. P. 2232–2239.

10. Hashim A., Wang L., Juneja K., Ye Y. et al. Vitamin B6s inhibit oxidative stress caused by Alzheimer's disease-related Cu(II)-βamyloid complexes-cooperative action of phospho-moiety // Bioorg. Med. Chem. Lett. 2011. Vol. 21. N 21. P. 6430–6432.

11. Kuwabara S., Nakazawa R., Azuma N., Suzuki M. et al. Intravenous methylcobalamin treatment for uremic and diabetic neuropathy in chronic hemodialysis patients // Intern. Med. 1999. Vol. 38. N 6. P. 472–475.

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15. Plecko B., Paul K., Mills P., Clayton P. et al. Pyridoxine responsiveness in novel mutations of the PNPO gene // Neurology. 2014. Vol. 82. N 16. P. 1425–1433.

16. Puighermanal E., Marsicano G., Busquets-Garcia A., Lutz B. et al. Cannabinoid modulation of hippocampal long-term memory is mediated by mTOR signaling // Nat. Neurosci. 2009. Vol. 12. N 9. P. 1152–1158.

17. Rehberg K., Kliche S., Madencioglu DA, Thiere M. et al. The serine/threonine kinase Ndr2 controls integrin trafficking and integrindependent neurite growth // J. Neurosci. 2014. Vol. 34. N 15. P. 5342–5354.

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21. Yao JJ, Sun J, Zhao QR, Wang CY et al. Neuregulin-1/ErbB4 signaling regulates Kv4.2-mediated transient outward K+ current through the Akt/mTOR pathway // Am. J. Physiol. Cell Physiol. 2013. Vol. 305. N 2. P. C197–206. n

Contraindications and side effects

The product has few contraindications. Taking Nootropil is completely excluded only in the presence of hemorrhagic stroke and severe kidney pathologies or acute failure. Another indicator of absolute contraindications is individual intolerance to piracetam or other substances included in the tablets, capsules or solution.

Pregnant and lactating women (at any stage) should use Nootropil with caution. Also, careful use is carried out in the presence of chronic diseases, acute conditions that disrupt homeostasis.

In some cases (especially often when the daily norm exceeds 5 g), taking Nootropil gives a number of side effects:

nausea;
vomit;
deterioration in concentration;
mood swings;
retardation of movements;
mental overexcitation;
sleep problems;
high level of anxiety;
appetite disorders;
gastralgia;
increased sexual desire;
headaches;
tremor;
dizziness.

Attention!

Taking the medicine may make your angina worse. Patients suffering from this disease should take the drug only under the supervision of a doctor and in accordance with the dosage.