Neuroprotectors helping restore cell health

nejroprotektory - Neuroprotectors helping restore cell health

Picamilon (sodium salt of N-nicotinol-y-aminobutyric acid) is rapidly absorbed in the digestive canal, easily penetrates the blood-brain barrier, is distributed in the brain, muscles and adipose tissue, excreted unchanged in the urine.

The presence in the chemical structure of picamilon GAM K and nicotinic acid determines its nootropic and vasoactive effect. It improves cerebral circulation and positively affects the metabolism of brain tissue. The drug also has antihypoxic, antioxidant and antiplatelet effects, has a tranquilizing effect, not accompanied by depression of the central nervous system, drowsiness, lethargy, muscle relaxation.

The mechanism of action of picamilon is due to its interaction with GABA receptors.

Indications for use: cerebrovascular accident, migraine, neurotic and neurosis-like conditions, asthenia, depression; assigned to restore performance after hard work in extreme conditions, increase resistance to physical and mental stress. In sports medicine, they are used to increase the body’s resistance to increased loads.

Side effects: allergic reactions, headache, dizziness, feeling of anxiety.

Glutamate antagonists

Glutamate antagonists are the primary agent used to prevent or control excitotoxicity in disorders of the central nervous system. The purpose of these antagonists is to inhibit the binding of glutamate to NMDA receptors, which will avoid the accumulation of Ca2 and, therefore, excitotoxicity. The use of glutamate antagonists is associated with enormous obstacles, since such treatment should overcome selectivity, since binding is inhibited in the presence of excitotoxicity. A number of glutamate antagonists have been investigated as agents for treating disorders of the central nervous system, but it has been found that many of them are ineffective or have unacceptable side effects. Glutamate antagonists are being intensively studied. The following are some of the treatments that may have promising results in the future:


The use of antioxidants as neuroprotectors is based on the inhibition of the reactions of non-enzymatic free radical oxidation of lipids and biopolymers, proteins, mucopolysaccharides and nucleic acids, followed by membrane-protective action, which ensures stabilization of structural integrity and preservation of the functional properties of neurons.

Mexidol (2-ethyl-6-methyl-3-hydroxypyridine succinate) is a derivative of 3-hydroxypyridine, in chemical structure it is an analogue of pyridoxine, the phosphorylated form of which has a neurotropic, antioxidant and energizing effect.

Emoxipin is a synthetic antioxidant; in its chemical structure, like Mexidol, it belongs to the group of 3-hydroxypyridines. Unlike Mexidol, it has a less pronounced antihypoxic effect, and also has angioprotective and antiaggregatory properties. It inhibits free radical oxidation of biomembranes, increases the activity of antioxidant enzymes and stabilizes the membrane structures of cells (red blood cells, platelets).

It slows down the free radical stages of the synthesis of prostaglandins catalyzed by cyclooxygenase and lipoxygenase and thus reduces the formation of thromboxane A and leukotrienes (LTB4 and others), prevents platelet aggregation and the development of thrombonecrotic outcomes of ischemic brain disease (strokes) and heart (myocardial infarction). Reduces the ratio of cholesterol/phospholipids, thereby reducing the viscosity of the lipid layer of the membrane.

Indications for use: ischemic and hemorrhagic disturbances of cerebral circulation, myocardial infarction, skin diseases, glaucoma and other diseases accompanied by activation of LPO processes. In ophthalmology it is used in the treatment of intraocular hemorrhages, angioretinopathies of various etiologies, including diabetic, for the protection and treatment of the cornea and retina of the eye when exposed to high-intensity light.

Side effects: agitation, drowsiness, moderate increase in blood pressure, skin rash, in the treatment of eye diseases – burning sensation, pain, itching, redness at the injection site.

Vitamin neuroprotective antioxidant effects (vit. E, C, P, etc.) are presented in the corresponding section.

Glutamic acid, glycine, lipoic acid increase the level of total and reduced glutathione. Glutamic acid has a neurotransmitter effect, stimulates redox processes, participates in protein and carbohydrate metabolism, helps neutralize and remove ammonia, increases tissue resistance to hypoxia, stimulates the synthesis of acetylcholine and ATP, and improves the transmission of excitation to the central nervous system.

Indications for use: epilepsy, psychosis, reactive depression, exhaustion. In sports medicine, it can increase tissue resistance to hypoxia during the recovery period.

!  A review of the disaggregants Aspirin, Clopidogrel, Prasegrel

Side effects: increased irritability, vomiting, diarrhea, anemia, leukopenia.

Glycine (glycosed-KMP) is a neurotransmitter of inhibitory type of action, a regulator of metabolic processes in the central nervous system, reduces psychoemotional stress, restores mental performance, has a neuroprotective, anti-stress, sedative effect, improves metabolic processes in the brain tissue, helps neutralize toxic products of ethyl alcohol oxidation, reduces the severity of asthenic syndrome, reduces the pathological craving for alcohol.

Indications for use: asthenic state, vegetovascular dystonia; It is used to increase mental performance, with psycho-emotional stress, various functional and organic diseases of the nervous system. It can be used in sports medicine: in the preparatory period to relieve psychomotor agitation.

Side effects: allergic reactions.

Lipoic acid also regulates lipid metabolism.

Xanthinol nicotinate (compliment) is a derivative of theophylline and nicotinic acid and combines their properties. The drug improves cerebral circulation, oxygenation of brain tissue, microcirculation, reduces platelet aggregation, blood viscosity, activates fibrinolysis.

The mechanism of action of compliance is due to inhibition of phosphodiesterase and the accumulation of cAMP. With prolonged use, the drug reduces the level of cholesterol, low and very low density lipoproteins and has an anti-atherosclerotic effect, which enhances its cerebroprotective properties.

The drug belongs to indirect antioxidants, increases the level of antioxidant activity of tissues, acts as a precursor of pyridine nucleotides, improves peripheral blood circulation, participates in oxidative de-carboxylation, activates lipid and carbohydrate metabolism, has antioxidant, lipid-lowering effect, improves liver function, has a detoxifying effect during intoxication.

Indications for use: atherosclerosis, neuropathy, intoxication, hepatitis, cirrhosis, cerebrovascular accident. In sports medicine, it is mainly used to improve microcirculatory processes and, accordingly, blood supply and tissue oxygenation.

Side effects: allergic reactions, dyspeptic disorders, decreased blood pressure, weakness, dizziness, hyperemia of the face and neck.

To normalize the blood circulation of the brain, drugs are used that improve the rheological properties of the blood, have a vasodilating effect, which leads to saturation of the brain tissue with oxygen and the elimination of ischemia.

Acetylsalicylic acid in low doses has an antiplatelet effect, the main mechanism of which is the inactivation of the cyclooxygenase-2 enzyme. This leads to impaired synthesis of thromboxane A2 in platelets and a decrease in platelet aggregation. The drug also exhibits indirect anticoagulant properties (disrupts the activation of coagulation factors in the liver – II, VII, IX, X) and inhibits the activity of plasminogen. It is effective for arterial thrombosis, since thrombi with a low fibrin content and a large number of platelets are formed in the arteries.

Acetylsalicylic acid is used to prevent cerebrovascular accident and stroke, coronary artery thrombosis, and to treat angina pectoris and myocardial infarction. The prophylactic dose is 100-300 mg-day “1. The drug can not be used if there is a history of erosive gastritis or peptic ulcer, since prolonged use can provoke gastric bleeding.

An alternative to aspirin is thienopyridine derivatives – clopidogrel (plavica) and ticlopidine (ticlide), they are used in case of impossibility or ineffectiveness of aspirin. Clopidogrel is currently prescribed in combination with aspirin. Combination therapy is more effective than monotherapy (aspirin).

Heparin is a direct-acting anticoagulant, which is explained by the ability of its high molecular weight chains to inhibit the key blood coagulation enzyme – thrombin. The drug is considered as an indirect inhibitor, since it requires coenzyme antithrombin III to carry out its anticoagulant action.

By binding to blood plasma antithrombin III and changing the conformation of its molecule, heparin significantly accelerates the initially slowed down binding of antithrombin III to the active centers of blood coagulation factors (IXa, XIa, XI 1a, kallikrein, and especially thrombin and factor Xa) and, as a result, their inactivation (inhibition of thrombosis).

On the contrary, when factor Xa is inactivated, heparin only interacts with antithrombin III, i.e., the amount of pentasaccharide residues in the molecule does not significantly affect its ability to accelerate it. It also forms a complex with antiplasmin, and thus increases the activity of the fibrinolytic system, and prevents platelet adhesion and aggregation.

Sincumar, warfarin, phenyline – indirect anticoagulants, antagonists of vitamin K, necessary for the formation of prothrombin in the liver. The drugs disrupt the biosynthesis of prothrombin, proconvertin (factor VII) and other blood coagulation factors (IX, X), enhance prostacyclin-synthesizing activity in the walls of blood vessels. Unlike heparin, they act slowly and continuously, they have a cumulative effect.

Indirect anticoagulants are used as neuroprotectors, for the prevention and treatment of venous thrombosis and embolism, with a thrombotic form of ischemic stroke.

Cinnarizine (stugeron) – N-benzhydryl-N-trans-cinnaluyl-piperazine) is a piperazine derivative.

!  First aid for acute left ventricular failure

Pharmacodynamics Cinnarizine improves blood circulation in the brain, coronary and peripheral blood circulation, has a high tropism to the vessels of the brain, reduces their spasm, response to pressor substances (norepinephrine, angiotensin, prostaglandins F2a, etc.), reduces platelet aggregation and blood viscosity, improves microcirculation and improves tissue resistance to hypoxia.

The mechanism of vasodilating action of the drug is associated with a blockade of Ca2 intake

through slow calcic channels and smooth muscle cells of the vascular wall. Cinnarizine is a selective type IV calcium channel blocker.

The vascular smooth muscle tone mainly depends on the concentration of cytoplasmic Ca2. In ischemia, hypoxia, and other pathological conditions, an increased concentration of Ca2 * can lead to spasm of the smooth muscles of the vascular wall, increased tissue oxygen demand, a significant increase in cellular metabolism, increased platelet aggregation, and various destructive processes.

Antioxidants are the main treatment used to control oxidation levels. Antioxidants act by eliminating reactive oxygen species, which are the main cause of neurodegradation. The effectiveness of antioxidants in preventing further neurodegradation is not only dependent on the disease, but may also depend on gender, ethnicity and age. The following are common antioxidants effective in reducing oxidative stress in at least one neurodegenerative disease:

Oxidative stress

Elevated levels of oxidative stress can be partially caused by neuroinflammation, which is part of brain ischemia, as well as many neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis. An increased level of oxidative stress is the goal of neuroprotective effects due to their role in the development of apoptosis of neurons.

Oxidative stress can directly cause the death of neuronal cells or can cause a cascade of events that leads to improper protein folding, proteosome dysfunction, mitochondrial dysfunction, or activation of glial cells. Any of these events causes neurodegeneration, since each of these events causes apoptosis of neural cells. 6) By reducing oxidative stress when taking neuroprotective agents, further neurodegeneration can be suppressed.

Application in sports medicine and in the practice of sports training

The ischemic process is considered as a universal mechanism of cell death. In order to prevent neuronal damage in ischemia, drugs with neuroprotective activity are used. The variety of mechanisms of action of the drugs allows, on the whole, to improve oxidative metabolism, reduce the processes of free radical oxidation and increase the activity of antioxidant defense, have a positive effect on neurotransmitters, and improve hemodynamics, which is especially important during intense physical exertion.

Neuroprotectors are effective means for the preventive pharmacological protection of nervous tissue in extreme conditions, with intense physical and mental stress, changing time and climate zones, which is observed during training, competitions, and neuro-emotional stress in athletes.


NMDA receptor stimulants can lead to excitotoxicity of glutamate and calcium and neuroinflammation. Some other stimulants, in appropriate doses, however, may be neuroprotective.

Other neuroprotective treatments

There are other neuroprotective treatment options that target different mechanisms of neurodegradation. Research is ongoing in an attempt to find some method effective in preventing the onset or progression of neurodegenerative diseases or secondary injuries. These include:

Detonic – a unique medicine that helps fight hypertension at all stages of its development.

Detonic for pressure normalization

The complex effect of plant components of the drug Detonic on the walls of blood vessels and the autonomic nervous system contribute to a rapid decrease in blood pressure. In addition, this drug prevents the development of atherosclerosis, thanks to the unique components that are involved in the synthesis of lecithin, an amino acid that regulates cholesterol metabolism and prevents the formation of atherosclerotic plaques.

Detonic not addictive and withdrawal syndrome, since all components of the product are natural.

Detailed information about Detonic is located on the manufacturer’s page

Editor-in-chief of the Detonic online magazine, cardiologist Yakovenko-Plahotnaya Tatyana. Author of more than 950 scientific articles, including in foreign medical journals. He has been working as a cardiologist in a clinical hospital for over 12 years. He owns modern methods of diagnosis and treatment of cardiovascular diseases and implements them in his professional activities. For example, it uses methods of resuscitation of the heart, decoding of ECG, functional tests, cyclic ergometry and knows echocardiography very well.

For 10 years, she has been an active participant in numerous medical symposia and workshops for doctors - families, therapists and cardiologists. He has many publications on a healthy lifestyle, diagnosis and treatment of heart and vascular diseases.

He regularly monitors new publications of European and American cardiology journals, writes scientific articles, prepares reports at scientific conferences and participates in European cardiology congresses.