Moderate cognitive impairment syndrome in old age: diagnosis and treatment

Impairments in intelligence, memory and other higher mental functions are a symptom of many neurological diseases. Such changes arise due to the deterioration of neuronal communication between brain cells due to their gradual necrosis against the background of hypoxia, chronic intoxication, and age-related changes. A complex of such disorders is called cognitive personality disorder. Unfortunately, in some cases they are irreversible, but with timely consultation with a doctor, the pathological process can be slowed down. In other cases, dysfunction is caused by completely treatable diseases, which is why doctors at the Leto clinic pay great attention to a comprehensive examination of the patient, and we select treatment tactics after consultation with highly specialized specialists.

Etiology

The main risk factor for the development of personality disorders with cognitive impairment is age. By the age of 65, almost 30% of patients who come for regular examinations to a therapist complain of a deterioration in intelligence. Risk factors include:

• hypertension: it has been proven that an increase in systemic blood pressure for every 10 mm Hg. increases the risk of intellectual dysfunction by 7–12%;
• coronary heart disease;
• arrhythmia;
• excess weight and physical inactivity;
• hyperlipidemia, atherosclerosis.

In addition, the causes of the syndrome may be:

• deficiency of vitamin B12, folic acid, thiamine;
• hepatic, uremic, discirculatory encephalopathy;
• endocrine pathologies: hypothyroidism, thyrotoxicosis, insulinoma (benign tumor that produces insulin);
• respiratory failure;
• alcohol or drug intoxication;
• autoimmune and systemic diseases, for example, lupus, sarcoidosis, vasculitis;
• some infections: neurosyphilis, HIV, neuroborelliosis, previous meningitis, encephalitis;
• hydrocephalus;
• brain tumors, aneurysms, surgical interventions;
• consequences of traumatic brain injury, stroke;
• depressive and anxiety disorders.

The listed diseases, although difficult, are treatable, and with the right treatment tactics it is possible to completely restore all intellectual processes. The prognosis is much worse if symptoms appear due to dementia or Alzheimer's disease. In such cases, only symptomatic treatment is possible.

Treatment for mild cognitive impairment

Treatment is designed to prevent the development of dementia, slow down the rate of cognitive impairment, and eliminate existing disorders. Treatment should be etiotropic, pathogenetic and include the use of antioxidants, antiviral neurotransmitters, vasoactive drugs, chemotherapy, surgical removal of the tumor, as well as correction of vascular disorders, depression, and dysmetabolic changes.

• Drug therapy is selected individually and includes metabolic agents and nootropics;
• Psychocorrection should be carried out regularly. This includes memorizing texts and poems, art therapy. Exercises can be carried out together with a psychologist, in a group or individually. The patient is taught to form semantic and situational connections and analyze. Monitoring the effectiveness of exercises and alternating them is necessary;
• It is also important to review your diet and daily routine. Middle-aged and older people need to reduce the amount of salt and fat they consume and increase the amount of antioxidants. It is important to maintain a daily routine that includes moderate physical activity, rational alternation of work and rest, and proper sleep. It is very important for the patient to remain socially active.

Medical prognosis

In most cases, with timely etiotropic treatment, the prognosis for most patients is positive. With a regressive course of the underlying disease, the disturbances can be reduced. Cognitive decline slows or stops.

Clinical forms and features of the course

The main cognitive functions include:

• attention: the ability to maintain a certain level of mental and emotional activity;
• memory: the ability to remember, save and reproduce information;
• praxis: purposeful motor activity;
• gnosis: perception and interpretation of color, smell, visual images, tactile sensations, sounds;
• speech: understanding the meaning of what is said, the ability to formulate and express one’s own thoughts; this group of functions includes reading and writing;
• management of thinking, emotions and behavior, cognitive activity, fulfillment of assigned tasks and goals.

With cognitive personality disorder, there is an objective and subjective deterioration of all of the above functions compared to the original ones. In this case, the use of generally accepted age criteria is considered incorrect, since patients differ in their level of intelligence in general or in individual abilities. For example, if a person has a photographic memory and unique logical thinking, what is considered average is a significant deterioration for him.

Main types of syndrome

There are several forms of the disease:

• subjective , in which complaints of memory impairment are not confirmed by detailed psycho-emotional testing;
• mild, accompanied by a slight, mild intellectual deficit, which is noted during a neurological examination, but such disorders do not affect everyday and professional activity;
• moderate: the most common variant of the disease;
• severe (cognitive-compulsive personality disorder), manifested by severe impairments with complete loss of even basic everyday skills.

Important! According to clinical studies, subjective, not confirmed by general examination, and mild cognitive personality disorders are sometimes the very first symptoms of Alzheimer's disease, so they should not be ignored in any case.

Moderate deficiency syndrome

It is with this form of pathology that people most often consult a doctor. Depending on the prevalence of certain symptoms in adults, the following types of disease are distinguished:

• Monofunctional amnestic , in which only memory suffers, other functions are not affected. This type of disorder is often a harbinger of Alzheimer's disease.
• Monofunctional non-amnestic. There are no complaints about memory impairment, but intellectual inertia occurs (decreased concentration, lack of motivation, slow thinking).
• Multifunctional amnestic. The pathology affects memory and several other cognitive functions.
• Multifunctional non-amnestic. The patient perfectly remembers what happened to him before, is able to assimilate and reproduce new information, but at the same time other types of higher mental activity are disrupted (for example, speech, visual-spatial perception, etc.).

Possible complications

Progressive MCI without timely effective therapy can develop into dementia, which leads to the loss of self-care skills and the ability to solve everyday problems. This gives rise to problems of socialization - the circle of contacts narrows, the ability to work is lost, and the desire to attend public events disappears. With a fluctuating course, patients have difficulty performing intense mental tasks, while correct correction of the daily routine and reduction of stress allows them to maintain their usual lifestyle.

Diagnostic examination of patients

If you suspect a cognitive personality disorder, it is recommended to do the following:

• general clinical analysis of blood and urine;
• biochemical blood test, including electrolytes, calcium, glucose, liver and kidney function indicators, lipid spectrum;
• tests to assess the hormonal profile, levels of B vitamins and folic acid;
• CT or MRI of the brain;
• serological testing for markers of syphilis and HIV (if symptoms of the disease appear at a young or mature age);
• according to indications: ECG, chest x-ray, duplex scanning of cerebral vessels, study of cerebrospinal fluid to detect markers of Alzheimer's and dementia.

To assess the severity of the pathology, psychological testing is carried out, which consists of the following points:

• orientation in place, in time and one’s own personality: the patient is asked to name the date and place of birth, say where he is, etc.;
• a test for repeating the names of objects (sometimes it is necessary to explain their meaning), individual numbers in order or randomly;
• Praxis assessment: they are asked to perform several conscious actions, for example, fasten buttons, fold clothes;
• tests of visual-spatial perception: the patient is asked to draw simple or three-dimensional geometric figures, depict a dial and mark a certain time with arrows;
• pay attention to the peculiarities of speech, the ability to maintain a conversation;
• assessing intelligence by searching for logical associations (for example, they suggest finding something in common between a plum and an apricot).

Cognitive impairment in neurodegenerative diseases

V.V. ZAKHAROV

, Doctor of Medical Sciences, Professor,
N.V.
VAKHNINA , Candidate of Medical Sciences,
Department of Nervous Diseases of the First Moscow State Medical University named after. I.M. Sechenova The review presents modern Russian and international data on the prevalence, genetic and environmental risk factors, pathogenesis, clinical picture, diagnosis and treatment of neurodegenerative diseases with cognitive impairment.
Among these, the most common are Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and frontotemporal degeneration (FTD). In the etiology of these diseases, the main role is played by genetic predisposition with a certain influence of external environmental factors. The role of metabolic disorders of cerebral proteins in the pathogenesis of neurodegenerative diseases is also being studied. The clinical picture in AD and FTD is represented by various cognitive disorders, in DLB – cognitive disorders in combination with motor and early psychotic disorders. In diagnostics, two types of neuroimaging, structural and functional, are becoming increasingly important, which make it possible to establish an accurate diagnosis at the earliest stages. Memantine and acetylcholinesterase inhibitors are used in the treatment of AD and DLB, and serotonergic drugs are used for FTD. Neurodegenerative diseases are the most common cause of cognitive impairment in old age. According to the laboratory of memory disorders of the Clinic of Nervous Diseases named after. AND I. Kozhevnikov, Alzheimer's disease ranks first in the list of causes of dementia and is responsible for approximately 40% of all cases of dementia [1]. Dementias associated with Lewy body degeneration (LBD) and frontotemporal degeneration (FTD) are also regularly encountered in clinical practice (Fig. 1). Neurodegenerative diseases are also thought to be responsible for the majority of cases of non-dementia cognitive impairment. However, there are currently methodological difficulties in recognizing the neurodegenerative nature of mild and moderate cognitive disorders. According to generally accepted operational criteria, a prerequisite for a definite diagnosis of AD, DLB, or FTD is the presence of dementia.

However, it is clear that clinically defined dementia is always preceded by less severe cognitive impairments that are not recognized or are mistakenly recognized as vascular.

Establishing an accurate nosological diagnosis of cognitive disorders is of great importance for prognosis and choice of therapeutic tactics. Therefore, clinicians need to have an understanding of the clinical features and paraclinical characteristics of neurodegenerative diseases accompanied by cognitive impairment. Alzheimer's disease

AD is the most common degenerative brain disease. It is assumed that BA is of a polyetiological nature. With the early onset of the disease, the leading etiological factor is genetic burden. Today, three pathological genes have been identified, the carriage of which provides an almost 100% risk of developing asthma before the age of 60 years. These include: the gene encoding amyloid precursor protein (chromosome 21), presenilin-1 (chromosome 14), and presenilin 2 (chromosome 1). The senile form of AD (onset after 60 years) is partially associated with another pathological gene - apoE4 (chromosome 19). The penetrance of this gene is not so high and, according to some data, is about 30%. In addition to genetic burden, risk factors for the development of AD are arterial hypertension, hyperlipidemia, hyperhomocysteinemia, diabetes mellitus, abdominal obesity, vitamin B12 deficiency, depression and a history of traumatic brain injury, a sedentary lifestyle, low levels of education and intellectual activity [2–6] .

A key link in the pathogenesis of AD is a violation of the metabolism of the amyloid precursor protein with the formation of a neurotoxic protein - beta-amyloid, which is deposited in the brain parenchyma and cerebral vessels. The experiment showed that beta-amyloid activates tissue mediators of inflammation, enhances the release of stimulating mediators (glutamate, aspartate, etc.), and promotes increased formation of free radicals. The result of this complex cascade of events is neuronal damage and death. In this case, different parts of the brain are involved in the pathological process unevenly. The death of the largest number of neurons in AD is observed in the hippocampus, temporal and parietal lobes, while damage to the frontal and occipital lobes occurs at later stages and to a lesser extent [4, 7–12].

The clinical picture of AD is characterized primarily by short-term memory impairments. At first, events of the immediate past are forgotten, then, as the disease progresses, amnesia spreads to more distant events [4, 13–15]. This pattern of progression of mnestic disorders is called Ribot's law. From the point of view of neuropsychology, memory impairment in AD is characterized by a number of specific features that make it possible to recognize this disease even in the absence of pronounced cognitive impairment (Table 1) [16, 17]. According to O.V. Uspenskaya and N.N. Yakhno, the presence of these neuropsychological features, as a rule, coincides with corresponding neurochemical changes in the cerebrospinal fluid already at the stage of moderate cognitive impairment [18].

At advanced stages of the disease, memory disorders are accompanied by impairments of other cognitive functions. Thus, disturbances in spatial orientation and insufficiency of the nominative function of speech, or amnestic aphasia syndrome, are very characteristic. In the advanced stages of AD, independence is lost, and behavioral disturbances may appear, such as increased suspicion and delusions of harm. At the end of the disease, patients are practically deprived of cognitive abilities and are completely helpless [13, 14].

The diagnosis of AD is valid in the presence of characteristic cognitive impairment and the absence of primary motor and sensory disorders. In recent years, methods for paraclinical diagnosis of asthma have been widely developed. Structural neuroimaging may show no changes or reveal cerebral atrophy, most pronounced in the hippocampus and temporal lobe cortex. Functional neuroimaging using positron emission tomography is more informative. This method at the stage of symptomatic asthma reveals glucose hypometabolism mainly in the temporoparietal regions of the brain. However, intravital detection of cerebral amyloidosis using a special ligand (the so-called Pittsburgh substance) is most specific. This method makes it possible to establish a diagnosis with a high degree of probability, including at the stage of asymptomatic (latent) asthma. Another approach to paraclinical diagnosis is a neurochemical study of cerebrospinal fluid. AD is characterized by a decrease in the content of amyloid protein and an increase in the level of tau protein. According to a number of leading international experts, the diagnosis of AD is legitimate in the presence of specific memory impairments and corresponding neuroimaging and/or neurochemical changes [17, 19].

Dementia with Lewy bodies

DLB was first described in the 70s of the last century by Japanese neurologists [20]. This form of neurodegenerative process is characterized by the appearance in the cytoplasm of cortical neurons of special inclusions - Lewy bodies, which contain alpha-synuclein and ubiquitin. Data on the prevalence of DLB ​​presented in various morphological studies vary from 12 to 27% [21–23]. Many researchers consider DLB to be the second most common cause of dementia in old age after AD. The etiology and pathogenesis of DLB ​​have been studied to a lesser extent compared to AD. However, as in AD, the leading trigger of the degenerative process is a disturbance in the metabolism of neuronal proteins [21, 23].

The clinical picture of DLB ​​is characterized by various combinations of cognitive, motor (extrapyramidal), behavioral and autonomic disorders. Cognitive impairments at advanced stages of the disease are represented by dementia, the foreground of which is impaired visual attention, spatial gnosis and praxis. Also characteristic are short-term and long-term memory impairments, slowing of cognitive processes (bradyphrenia), and impairment of frontal control functions (goal setting, planning and control) [24 – 28].

DLB is characterized by extrapyramidal motor symptoms, such as shortened step length, shuffling, and difficulty initiating walking. Other symptoms of parkinsonism may be observed: hypokinesia, rigidity, and disturbances in postural stability. Typically, extrapyramidal symptoms are symmetrical, less often they predominate on one side, reminiscent of classic Parkinson’s disease. Tremor is absent or occurs during postural and kinetic loads, which distinguishes it from the classic resting tremor characteristic of PD. Another characteristic manifestation is autonomic failure in the form of orthostatic hypotension, chronic constipation, urinary disorders, etc. [21, 29–31].

Behavioral disorders in DLB are manifested by repeated visual illusions and hallucinations, usually in the form of living images - animals or people. Hallucinations occur already at the stage of mild dementia. At the same time, criticism towards them at the beginning of the disease is, as a rule, intact, but over time it may become impaired. In the most severe cases, vivid, recurring hallucinations are combined with confusion and a sharp increase in the severity of cognitive and motor impairments [32, 33].

DLB is also characterized by spontaneous fluctuations in the severity of symptoms – the so-called. fluctuations. At the same time, for no apparent reason, the severity of cognitive, behavioral and motor disorders increases. Subsequently, spontaneous recovery of function is observed, which can be complete or partial. DLB is characterized by both short-term fluctuations, when symptoms fluctuate within one day, and long-term ones, lasting up to several weeks [22, 24].

The diagnosis of DLB ​​is based on a characteristic combination of cognitive, extrapyramidal motor and behavioral disorders, and the presence of fluctuations. An MRI of the brain reveals a picture of cerebral atrophy, with a relatively specific sign being a significant expansion of the posterior horns of the lateral ventricles (Fig. 2). The generally accepted diagnostic criteria for DLB are shown in Table 2 [34 – 36]. Frontotemporal degeneration

FTD is a degenerative process that primarily affects the frontal and/or temporal lobes of the brain, often on one side. According to epidemiological data, 5–10% of dementias are caused by frontotemporal degeneration. Unlike asthma and DLB, FTD often begins at a presenile age (50–65 years). This disease is the second most common cause of dementia after AD in patients under 65 years of age [37, 38].

FTD is a genetically determined disease, although sporadic cases are not uncommon. Family forms are characterized by an autosomal dominant type of inheritance. The pathogenesis of FTD is based on disruption of the metabolism of tau protein and ubiquitin, which leads to damage to the neuronal cytoskeleton and neuronal death. The morphological picture of FTD is a histochemically heterogeneous group of neurodegenerative changes, which are most pronounced in the frontal and anterior temporal lobes of the brain [39].

There are two main clinical variants of FTD. In the most common – “behavioral” – variant, the first symptom of FTD is a decrease in criticism. The patient begins to behave inappropriately to the rules of behavior accepted in this society, the sense of distance decreases, and tactfulness is lost. At the same time, there is a decrease in motivation and initiative, which is manifested by a loss of interest in work, family, and previous hobbies. Sexual incontinence, increased appetite, especially cravings for sweets, and alcoholic excesses may appear. Patients stop taking care of their appearance and become sloppy and unkempt. Foolishness, flat and inappropriate humor are often noted, irritability and aggressiveness may appear. At the same time, unlike AD and DLB, long-term memory remains intact for a long time. In the early stages of FTD, formal neuropsychological tests, especially rapid methods (Mini Mental State Examination, Clock Drawing Test), do not always reveal any significant cognitive impairment, despite the presence of undoubted behavioral disturbances. Simultaneously with behavioral disorders, changes in the emotional sphere develop. The most characteristic are emotional dullness and affective flattening, which are often mistaken for depression. Emotional lability, which is manifested by rapid and causeless changes in mood, is also common. A true decrease in background mood has also been described [40, 41].

The second clinical variant of FTD is characterized by isolated or almost isolated speech disorders (onset as primary progressive aphasia). With predominant damage to the left frontal lobe, patients become laconic, speech production is reduced mainly to monosyllabic answers to asked questions, and rare spontaneous statements acquire a specific “telegraphic style.” In general, the picture of speech disorders corresponds to dynamic aphasia. Cases of mutism have also been described, when speech production is completely absent. The predominant involvement of the left temporal lobe in the pathological process is characterized by insufficiency of the nominative function of speech, the disappearance of nouns from the patient’s speech production, and then a violation of the recognition of nouns in addressed speech [42–44].

Regardless of the type of onset of FTD (behavioral, speech), both behavioral and dysphasic disorders are usually present at the advanced stage of the disease.

Primary motor and sensory disturbances are not typical for FTD, although the neurological status may reveal physical signs of frontal dysfunction: revitalization of oral automatism reflexes, the phenomenon of resistance, grasping reflexes. In extremely rare cases, FTD is combined with the syndrome of parkinsonism and/or amyotrophic lateral sclerosis (parkinsonism-ALS-dementia symptom complex) [45].

The diagnosis of FTD is primarily clinical and is based on the dominance of behavioral and emotional disturbances at the onset of the disease with relative preservation of memory for current events. Neuroimaging methods in most cases reveal local atrophy of the frontal and/or temporal regions, often unilateral or asymmetrical [46, 47]. However, these neuroimaging changes are not necessary for diagnosis. Single photon emission computed tomography can detect hypoperfusion predominantly in the anterior parts of the brain [48]. Commonly accepted diagnostic criteria for FTD are shown in Table 3 [49, 50].

Differential diagnosis of neurodegenerative diseases with the clinic of cognitive impairment

All neurodegenerative diseases are characterized by a gradual, insidious onset. Often, neither the patient nor his relatives notice cognitive and behavioral disorders for a long time until they develop a clear dependence on others. Subsequently, patients and their relatives often experience difficulties when trying to retrospectively establish the exact time of onset of the disease.

A common characteristic of various neurodegenerative diseases is also the tendency for continuous progression. The rate of progression can be different: the highest rate is observed in DLB, the average in AD and the lowest in FTD. Temporary cessation of progression and prolonged stationary states are not typical, but are possible, and do not exclude the diagnosis of a neurodegenerative disease, especially in very elderly and geriatric patients.

Differential diagnosis between different forms of the neurodegenerative process is based on neuropsychological characteristics, characteristics of emotional and behavioral status, the presence and clinical characteristics of primary movement disorders, and neuroimaging data. The main differential diagnostic features are given in Table 4.

In old age and senility, the same patient may experience two cerebral diseases simultaneously. Morphological studies indicate that approximately 10% of patients with AD additionally have Lewy bodies, and 30% of patients with DLB have senile plaques and neurofibrillary tangles characteristic of AD. The clinical picture in such patients may contain signs of both diseases [7, 9, 11, 12, 25].

Treatment of cognitive impairment in neurodegenerative diseases

AD and DLB are characterized by very similar neurochemical changes. Therefore, for these diseases, a general therapeutic approach is used. The drugs that affect synaptic transmission processes have proven themselves better than others: cerebral acetylcholinesterase inhibitors and memantine (Akatinol Memantine). The effectiveness of these drugs in the treatment of cognitive disorders has now been fully proven, therefore acetylcholinergic drugs and Akatinol Memantine are the standard of care for patients with AD and DLB. In relatively small studies, carried out mainly in the 70–80s. XX century, the positive effect of some vascular and neurometabolic drugs was also demonstrated, which can be considered as second-line drugs in the initial stages of AD and DLB [51–53].

The use of acetylcholinesterase inhibitors is based on the acetylcholinergic hypothesis of cognitive impairment. Back in the 80s. XX century It has been shown that the severity of cognitive impairment in AD significantly correlates with the activity of acetylcholine transferase, the enzyme that synthesizes acetylcholine. The results of clinical studies confirmed the effectiveness of cerebral acetylcholinesterase inhibitors in AD with mild to moderate dementia. Against the background of their use, there is a decrease in the severity of both cognitive and emotional-behavioral disorders, an increase in the degree of independence of patients in everyday life, and an improvement in the quality of life of patients and their relatives. Currently, three acetylcholinesterase inhibitors are used to treat AD: donepizil, rivastigmine and galantamine [51–53]. Studies have also proven the effectiveness of acetylcholinergic drugs in DLB [22, 34].

Another strategy for the treatment of AD and DLB is to reduce the activity of the glutamatergic cerebral system. Glutamate is an excitatory transmitter, the release of which increases the energy expenditure of the postsynaptic neuron. It is known that beta-amyloid, which accumulates in the brain parenchyma in Alzheimer's disease, promotes increased release of glutamate into the synaptic cleft. An increase in the activity of the glutamatergic system is also observed in DLB. An increase in glutamatergic influences inevitably leads to depletion of the neuron's energy resources, resulting in instability of the membrane potential and cell death. It follows from this that to ensure neuroprotection it is necessary to reduce the activity of the glutamatergic system or increase the threshold for generating the excitation potential of the postsynaptic membrane. The latter can be achieved by blocking postsynaptic NMDA receptors for glutamate. However, this blockade should be reversible, since normal transmission of excitation through the glutamatergic synapse plays an important role in ensuring memory and attention processes [4, 51, 53–56].

Memantine (Akatinol Memantine) is a reversible blocker of postsynaptic NMDA glutamate receptors. The drug helps to increase the threshold for generating the excitation potential of the postsynaptic membrane, but does not lead to complete blockade of the glutamatergic synapse. In other words, when memantine is used, increased concentrations of glutamate in the synaptic cleft are required for the transmission of excitation. Since in AD and DLB the activity of the glutamatergic system increases and more transmitter is released into the synaptic cleft, exposure to memantine leads to normalization of glutamatergic transmission. According to N.N. Yakhno and O.V. Uspenskaya, the use of Akatinol Memantine in patients with the amnestic type of mild cognitive impairment syndrome is accompanied by positive dynamics of neurochemical parameters in the cerebrospinal fluid, which indirectly confirms the neuroprotective effect of the drug [57].

Normalization of the stereotype of glutamatergic transmission under the influence of Akatinol Memantine has both a neuroprotective and positive symptomatic effect, not inferior to the effect of acetylcholinesterase inhibitors. It should be noted that in Germany, Akatinol Memantine has been successfully used to treat primary degenerative and vascular dementia for about 30 years. In the 90s XX and early XXI centuries. A large series of international randomized studies of Akatinol Memantine were conducted using a double-blind method, during which the effectiveness of the drug was convincingly proven in accordance with the requirements of modern evidence-based medicine. The above-mentioned clinical studies have confirmed that the use of Akatinol Memantine improves cognitive functions, normalizes the behavior of patients with asthma of varying severity, increases their degree of independence in everyday life, and reduces the burden associated with caring for patients for their relatives [54–56].

The advantage of Akatinol Memantine is its high safety of use and good tolerability. The drug does not affect heart rate, can be used in therapeutic doses for liver and kidney diseases, and does not cause gastrointestinal disorders. In rare cases, the drug may have a mild psychoactivating effect, so it is not advisable to take it before bed. Limitations to the use of memantine are uncontrolled epilepsy and disturbances of consciousness.

Akatinol Memantine can be prescribed as monotherapy or in combination with acetylcholinesterase inhibitors. According to some data, combination therapy has the most pronounced positive effect on cognitive functions [56]. There are no drug interactions between these drugs, therefore, in combination therapy, the drugs are used in normal therapeutic doses (Fig. 2).

There is currently no effective treatment for FTD. Acetylcholinesterase inhibitors do not have a therapeutic effect in this disease, and the use of Akatinol Memantine has not been studied. According to some data, selective serotonin reuptake inhibitors have a moderate positive effect on behavioral disorders [58, 59].

Thus, neurodegenerative diseases with cognitive impairment are a group of very common diseases that are currently being actively studied. Thanks to the development of new therapeutic approaches, some progress has been made in the treatment of AD and DLB. Modern neurotransmitter therapy can reduce the severity of main symptoms, such as cognitive and behavioral disorders, and increase the level of functional independence of patients. Advances in clinical and basic neurobiological sciences may make it possible in the foreseeable future to stop the progression of the neurodegenerative process at its earliest stages.

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Cost of services

This list does not contain all prices for services provided by our clinic. The full price list can be found on the “Prices” , or by calling: 8(969)060-93-93. Initial consultation is FREE!

Principles of treatment

Therapy is prescribed only after receiving the results of a diagnostic examination. But usually treatment is aimed at:

• normalization of cerebral circulation, improvement of energy metabolism in brain cells, prevention of hypoxia;
• prevention of neurodegenerative changes;
• compensation for deficiency of B vitamins and other macro- and microelements, essential amino acids;
• therapy for concomitant disorders (use of antihypertensive and antiarrhythmic drugs, hepatoprotectors, etc.).

If the cause is not eliminated, cognitive personality disorder will progress: if in a mild form of the syndrome the patient only needs help managing finances and paying for utilities, at the stage of severe dementia the patient is completely dependent on others. In such cases, we offer hospitalization in our hospital, where the person will be under round-the-clock supervision by qualified and experienced medical personnel.

You can call a doctor or make an appointment at a clinic with our operators using a 24-hour anonymous phone number 8(969)060-93-93.

Cognitive potential in practical life

Today, many people do not read books due to wasted time on social networks and the Internet. Thus, a person does not develop cognitive abilities, and cannot achieve great heights in his skills and abilities. Thus, a person in practical life often does not know where to go to study in order to get a profession and education. Statistics show that in the CIS countries 80-90% of people do not work in their profession, and they chose the wrong educational institution. The whole problem is cognitive failure to choose the right person to become. The situation is similar with jobs. Many people work in one place for a very short period of time because the job they choose is not suitable for them. Many people often have no idea how they will succeed in life due to the fact that many become a gray mass “swimming with the flow.” The whole reason is weak cognitive potential, which does not develop for various reasons. This is just a short series where many make a mistake without realizing it. The sphere of relationships, finances, time, choice of material things, use of resources. Due to many mistakes in these important areas, a person's overall quality of life suffers.

5 most effective ways of cognitive development

We offer 5 key steps for cognitive development after reading this article.

1. Discipline. This is a broad concept that manifests itself from small things to global things. How you wake up in the morning and how early you go to bed will determine your entire day. Body training and brain exercises are important every day because the body needs stress. Achieving the right goals leads you to overall success in life.
2. Proper nutrition. Health is nutrition, and without health, the quality of life and development becomes dramatically more difficult. Therefore, take care of proper nutrition, drink more clean water and do not abuse bad habits. Better yet, give them up.
3. Read educational literature more than social networks. Today there are many excellent materials on how to improve the quality of life by working and analyzing many areas of life. Practice and find out what can be useful to you from simple things to more complex ones.
4. Develop your brain narrowly. Memory, thinking and concentration are key in brain development. The Mozgotren service is capable of effectively and most importantly quickly developing the brain at these three levels. For motivation in the service, you can track your rating and statistics.
5. Get quality rest. The modern problem of humanity is the inability to rest, and this gives rise to constant fatigue and depression. Today people go on vacation, but their heads are full of business and news from the Internet. Learn to disconnect from virtual and online reality to restore strength for further achievements.

To summarize, it is worth saying that developing balanced cognition today is not difficult. It is only important to direct your time and potential in the right direction by training your brain, and not waste your energy in the wrong direction, which is suggested by various advertisements. Don't miss the opportunity to live effectively, because otherwise your life will be lived by others.