The main problem associated with Alzheimer's disease- inattention of the patient’s relatives to the first alarming symptoms, which they frivolously attribute to banal aging. In order to avoid catastrophic consequences, we recommend immediately contacting the National Center for Clinical Psychiatry, where all conditions have been created for an in-depth diagnosis of the stage of the disease and the nature of the pathological process, as well as the most effective treatment, allowing the patient to prolong his stay in society as a full-fledged member of it.

Diagnosis of Alzheimer's disease at the National Center for Clinical Psychiatry.

If you suspect Alzheimer's disease The NDC patient will first of all undergo an examination and... His medical history will be carefully analyzed, as well as information about the mental health of his relatives. The primary diagnostic criterion in this case is gradual memory loss and weakening of cognitive abilities. It is necessary to establish the current functional state of the brain, and, if necessary, the thyroid gland. The Center's staff includes highly qualified diagnostic doctors, whose experience largely determines the further success of treatment. List of diagnostic measures to identify Alzheimer's disease and the development of individual tactics for its treatment includes, and, a blood test for thyroid hormones, and neuropsychological tests.

Treatment of Alzheimer's disease.

The NDC does not reassure patients’ relatives, making empty promises: yes, Alzheimer's disease truly incurable. But by adequately and competently constructing the therapeutic process, one can (and should) achieve a significant mitigation of symptoms, slowing down further progression of the disease and the maximum possible socio-psychological adaptation of the patient in society under the current circumstances. cornerstone Alzheimer's disease treatment at the NDC of Clinical Psychiatry is drug therapy: based on a series of diagnostic tests, the patient is offered an individual drug regimen that meets his individual needs and current condition. Depending on the situation, combinations are used, including type B monoamine oxidase inhibitors, 2nd generation acetylcholinesterase inhibitors, neuroprotectors (memantine), NSAIDs, vitamins, and symptomatic therapy. The National Center for Clinical Psychiatry is in close contact with the best Israeli clinics, exchanging experiences and their own best practices. Examples of such productive cooperation are the Israeli computer program Savion, the purpose of which is to help the patient remember individual episodes from the past, and the NeuroAD electromagnetic therapy device, which allows restoring some behavioral functions.

Prevention of Alzheimer's disease.

NDC guarantees all its patients constant psychological support, which is very important for patients suffering from Alzheimer's disease, and is an important part of the prevention of this disease. Ours will not let the brain of an elderly person with Alzheimer's disease, constantly training him and keeping him in constant tone. To do this, we use memorizing poetry, solving crosswords, and learning foreign languages. This should also include moderate physical activity and dietary adjustments (our “secret weapon” for prevention of Alzheimer's disease- so-called Mediterranean diet).

In conclusion, it should be noted that NDC specialists are constantly searching for effective methods Alzheimer's disease treatment, which undoubtedly inspires optimism and gives hope to our patients and their relatives.

Unfortunately, vascular lesions of the brain and primary degenerative disorders are often combined. In these cases, it is customary to talk about mixed dementia.

According to numerous studies, at least half of patients with Alzheimer's disease suffer from disorders of the circulatory system of the brain. Along with this, approximately 75% of patients diagnosed with vascular dementia experience symptoms of neurodegenerative processes.

This connection is quite understandable. Alzheimer's disease is asymptomatic for a long time (on average about 20 years). The brain is a fairly flexible instrument and for a long time compensates for the negative processes associated with the death of neurons. Stroke and coronary artery disease reduce the reserve and accelerate the onset of Alzheimer's type dementia. The inverse relationship is also quite obvious. Alzheimer's disease increases the risk of vascular diseases of the brain, since the deposition of beta-amyloid (senile plaques) occurs both in the brain itself and on the walls of blood vessels, leading to their damage (angiopathy).

What causes mixed dementia?

Primary degenerative processes and vascular diseases have many common prerequisites. These include:

• carriage of the APOE4 gene;
• high blood pressure;
• cerebral atherosclerosis;
• arrhythmias;
• high cholesterol;
• bad habits (poor diet, smoking);
• physical inactivity.

Thus, the frequent combination of Alzheimer's disease and vascular dementia is quite natural.

Diagnosis of the disease

Suspicion of mixed dementia is appropriate in cases where the appearance of cognitive disorders of the Alzheimer's type (primarily memory impairment) is preceded by cardiovascular diseases (hypertension, atherosclerosis).

An atypical set of symptoms allows one to suspect mixed dementia. For example, if memory problems are not combined with disturbances in spatial orientation, as often happens in Alzheimer's disease, but are accompanied by problems more characteristic of diseases associated with dysfunction of the frontal lobes: these are difficulties concentration, impaired ability to plan one’s actions, slowness when performing intellectual work.

Treatment

Treatment of mixed dementia combines correction of vascular factors (primarily gradual normalization of blood pressure, antiplatelet therapy) and the use of anti-dementia drugs.

The material was prepared by the Memini project.

Alexander Sonin

According to unofficial data in Russia, 80% of patients over the age of 65 suffer from dementia. Considering the fact that more than 2.5 million elderly people live in the capital, the treatment of Alzheimer's disease in Moscow is becoming a serious problem.

Symptoms

The disease is a form of progressive dementia (dementia), leading to loss of ability to learn new things. An elderly patient loses all previously acquired skills and experiences:

• forgetfulness;
• incoherent speech and speech disorders;
• inability to communicate;
• delusions, hallucinations;
• aggressiveness or, conversely, complete apathy;
• loss of orientation in familiar places;
• inability to recognize family and friends.

In addition, the person experiences urinary and fecal incontinence, difficulty walking, and difficulty performing usual daily activities.

Typically, Alzheimer's disease develops in several stages in older people. The first stage, when the only characteristic feature is the inability to remember new information, is often mistaken for natural age-related changes. Gradually the symptoms worsen. The last stage - the patient loses speech functions, cannot perform any actions and practically does not get out of bed, physical and mental exhaustion and disability occur.

Reasons

The disease is a consequence of a dysfunction of the central nervous system. Until now, medicine has not been able to identify the exact cause of degenerative changes. There is a theory that this disorder is a pathology of chromosomes, in particular the 1st, 14th, 19th, 21st. But since the phenomenon has not been fully studied, it is generally accepted that the development of the disease can be triggered by:

• heredity;
• arterial hypertension;
• cerebral atherosclerosis;
• diabetes mellitus;
• Down syndrome.

According to the observations of doctors, people with a low level of intelligence, insufficient physical activity, who are overweight, and with frequent depression are most susceptible to the disease.

There is currently no way to cure Alzheimer's disease. In Moscow, according to official data, over 100 people die from this disease every year; the real picture is 5-6 times higher.

Diagnosis and supportive therapy

Prevention of the development of the disease in old age is intellectual activity, dietary nutrition, and timely treatment of cardiovascular diseases. But if prevention does not produce a positive result, it is very important to consult a psychotherapist if you detect signs of changes in cognitive behavior or memory impairment in an elderly person.

To diagnose the disease, the medical history of the patient and his relatives is studied. A psychotherapist conducts neuropsychological testing to identify the patient’s intellectual abilities. X-ray studies (CT, MRI, PET scan, puncture) help identify signs of pathology in the brain and spinal cord.

If a specialist says he knows how to treat Alzheimer's disease, run away from him. Because when a positive diagnosis is made, the doctor’s efforts are aimed at slowing the progression of the disorder and nothing more. For this purpose, medications are prescribed and psychological sessions are conducted. These measures are not treatment as such. They are intended to alleviate symptoms and adapt to the disease.

Providing proper care is the foundation of the entire program. Creating a constant routine, safety, proper nutrition, timely reminders of physiological needs and other actions will ensure comfort and peace for the elderly person and his family.

If you don’t know which doctor treats Alzheimer’s disease, contact psychotherapist I.G. Gernet (Moscow). Many years of experience in psychiatry allows him to give effective recommendations regarding the prevention of the initial stage, use proven diagnostic methods, proven methods of psychotherapy and effective medications. The doctor will give practical advice on patient care, help an elderly patient adapt to new conditions, make a home visit if necessary, and give advice over the phone. By using the services of a specialist, you can give your elderly loved ones a few more years of normal life.

Definition. Alzheimer's disease [AD] is the most common form of primary (genetically determined) degenerative (i.e., caused by the gradual death of neurons in the cerebral cortex) dementia of late age (up to 60 - 70% of all cases of dementia), which is characterized by a gradual, subtle onset in presenile or old age, the steady progression of memory disorders and higher cortical functions (praxis, gnosis, speech, intelligence) up to the total collapse of mental activity as a whole, as well as a characteristic complex of neuropathological and neurochemical signs (synonymous with AD - dementia of the Alzheimer's type).

read also the article: Dementia(to the site)

Etiology(and risk factors). In hereditary forms of AD, the main genes responsible for its development are: the gene encoding the amyloid precursor protein (APP, chromosome 21), genes encoding enzymes (the so-called alpha, beta and gamma secretases), which, in turn, metabolize APP: presenilin 1 (chromosome 14), presenilin 2 (chromosome 1). In sporadic forms of asthma, hetero- or homozygous carriage of the 4th isoform of the apolipoprotein E gene (ApoE 4) deserves special attention - in such patients, asthma develops earlier and usually has a more malignant course than in people with the 2nd or 3rd isoforms of ApoE (ApoE is a protein with multiple functions, which is expressed in the brain, but not in neurons, but in glial cells; ApoE is involved in regeneration processes during damage to the central nervous system; the participation of ApoE in compensatory cholinergic synaptogenesis has been proven; the relationship between the ApoE genotype and cholinergic deficiency has been shown in AD: a decrease in acetylcholine transferase activity in the hippocampus and temporal cortex is inversely proportional to the number of copies of the ApoE4 gene allele; the mechanism of participation of the ApoE gene in the genesis of AD is unclear).

It should be noted that the development and progression of asthma are determined by genetic factors in only 10% of all patients with asthma (the so-called “pure” asthma, or early-onset asthma). In other cases, the rate of development of the neurodegenerative process is influenced by many (risk) factors. Old age is the strongest risk factor for AD. The peak incidence of asthma occurs in the 80-90 years of life: crossing the 80-year mark triples the risk of developing this disease (the prevalence of asthma among people over 85 years of age is 25-30%). A family history of this disease is also of great importance, especially if it begins before the age of 65 years. It is believed that the risk of developing asthma is 4 times higher in close relatives of patients and 40 times higher if there are two or more cases of dementia in the family. According to epidemiological data, about 30% of patients with asthma have relatives with asthma. A family history of indications for Down syndrome is also a risk factor for the development of asthma. Other factors that increase the risk of developing asthma include: uncontrolled arterial hypertension in middle and old age, atherosclerosis of the main arteries of the head, hyperlipidemia, hyperhomocysteinemia, diabetes mellitus, overweight, physical inactivity, chronic hypoxia (for example, in diseases of the respiratory tract), cranial history of brain injury, low level of education, low intellectual activity throughout life, episodes of depression in young and middle age, female gender.

Pathogenesis. The starting point of the pathogenesis of AD (according to the most discussed “amyloid hypothesis”) is a violation of the metabolism of the amyloid precursor protein (APP). The currently identified AD genes (see above) either directly encode this protein or enzymes that metabolize it. Normally, PAB is cleaved by the enzyme alpha-secretase into polypeptides of equal size that are not pathogenic. If this protein is genetically defective or the enzyme systems are defective, PAB is cleaved by beta- and gamma-secretases into fragments of different lengths. In this case, long fragments (alpha-beta-42) are insoluble and are therefore deposited in the brain parenchyma and the walls of cerebral vessels (stage of diffuse cerebral amyloidosis). Next, in the brain parenchyma, aggregation of insoluble fragments occurs into a pathological protein - beta-amyloid. “Nested” deposits of this protein in the brain parenchyma are called senile plaques. Deposition of amyloid protein in cerebral vessels leads to the development of cerebral amyloid angiopathy, which is one of the causes of chronic cerebral ischemia.

read also the article: Amyloidosis(to the site)

Beta-amyloid and insoluble fractions of diffuse amyloid protein have neurotoxic properties. The experiment showed that against the background of cerebral amyloidosis, tissue inflammatory mediators are activated, the release of stimulating mediators (glutamate, aspartate, etc.) increases, and the formation of free radicals increases. The result of this entire complex cascade of events is damage to neuronal membranes, which is indicated by the formation of neurofibrillary tangles (NFTs) within the cells. NSF are fragments of a biochemically altered inner membrane of a neuron and contain hyperphosphorylated tau protein. Normally, tau protein is one of the main proteins in the inner membrane of neurons. The presence of intracellular NSFs indicates irreversible damage to the cell and its rapid death, after which NSFs exit into the intercellular space (“NPS-ghosts”). The neurons surrounding the senile plaques are the first and most affected.

Thus, the pathological anatomy of asthma is represented by three main types of changes: [ 1 ] senile plaques, [ 2 ] intracellular NSF and [ 3 ] cerebral atrophy. Cerebral atrophy is manifested by a decrease in the volume and weight of the brain, expansion of the cortical grooves and the ventricular system (the greatest severity of atrophic changes is noted in the hippocampus and the functionally connected deep parts of the temporal lobes of the brain; then pathological changes consistently develop in the posterior parts of the temporal lobes and in the parietal lobes of the brain brain; a relatively early event in the pathogenesis of AD is damage to the nucleus of Meynert and the innominate substance, which are the beginning of the ascending acetylcholinergic pathways in various parts of the brain; the convexital parts of the frontal cortex and primary motor and sensory areas are most recently involved in the pathological process).

It should be noted that the initial signs of Alzheimer's degeneration, such as diffuse cerebral amyloidosis and even senile plaques, are found in the vast majority of old people with normal cognitive functions for age. Therefore, a mandatory morphological criterion for the diagnosis of AD is the presence of not only early, but also late signs of AD, such as NFS and neuronal death. The severity of the changes also matters. Moreover, the degree of cognitive impairment correlates with a decrease in the number of neurons and synapses between them and does not correlate with the severity of cerebral amyloidosis. The presence of another concomitant pathological process in the brain, even slightly expressed, leads to the clinical manifestation of dementia syndrome at earlier stages of the degenerative process. We are talking primarily about cerebral vascular insufficiency, which shortens the preclinical phase of asthma and transforms an asymptomatic process into a symptomatic one. This is probably why AD shares common risk factors with cerebrovascular pathology (arterial hypertension, atherosclerosis, hyperlipidemia, hyperhomocysteinemia, diabetes mellitus), and timely correction of these disorders leads to a delay in the onset of dementia. From the onset of morphological changes in the brain to the development of the first symptoms of the disease, approximately 10 - 15 years pass.

Clinic. There are two clinical types of asthma: [ 1 ] AD with early onset (conditionally before 65 years, but more often at the age of 40 - 55 years; synonyms: type 2 AD, presenile dementia of the Alzheimer's type) develops mainly at presenile age, is accompanied by a steady progression of impairments in memory, intellectual activity and higher cortical functions and leads to the development of total dementia with severe disorders of speech, praxis and optical-spatial activity (afato-apractic-agnostic dementia); [ 2 ] AD with late onset (conditionally after 65 years; synonyms: type 1 AD, senile dementia of the Alzheimer's type) begins in the vast majority of cases in senile or (less often) elderly age with subtle memory impairment, general intellectual decline and personality changes, further with steady progression develops total dementia of the amnestic type, accompanied by a general decrease in higher cortical functions, which (unlike presenile AD) relatively rarely reach the level of severe cortical focal disorders; carriage of the 4th isoform of the ApoE gene (ApoE4) is currently recognized as the main genetic risk factor for the development of late-onset AD; [ 3 ] in addition, provision is made for the identification of atypical asthma or mixed type dementia, i.e., a combination of manifestations characteristic of asthma and vascular dementia. The average duration of asthma is 8 - 10 years, but it can be longer, protracted (up to 20 years) or catastrophic - from 2 to 4 years.

Remember! When clinical symptoms of the disease appear, special attention should be paid to the nature of memory impairment. Memory impairment is the first symptom of the disease. Typically, impaired recall of recent events, although with the development of the disease, memory of distant events is lost, and then recall of key moments in life (marriage, name of spouse, number, names and dates of birth of children, profession, own name and date of birth). Memory impairments are of a special “hippocampal” nature - when memorizing words or visual images, the patient has a reduced volume of delayed (after 5 minutes or more) reproduction of information compared to immediate (immediately after memorization). Organizing techniques (hints that help you learn material) do not make memorization easier. When reproducing memorized material, “extraneous interweavings” are noted - for example, the patient can name words that he did not learn.

Diagnostics. Currently, asthma can be diagnosed before clinical symptoms develop. Thus, using magnetic resonance imaging (MRI) in AD, it is possible to detect a decrease in the volume of the hippocampus, amygdala, medial temporal lobe, and posterior cingulate gyrus. The severity of atrophy usually does not correlate with the severity of symptoms of the disease when the clinical picture of AD is already formed, but neuroimaging data can be useful as an additional sign confirming the disease. When performing functional neuroimaging, it is possible to establish a diagnosis of AD with a high degree of certainty, including at the preclinical stages of the disease. Thus, positron emission tomography () with the Pittsburgh substance (PIB) can detect the accumulation of amyloid protein in cerebral structures before the development of symptoms of memory impairment. At the clinical stages of AD, identifying functionally hypoactive areas of the cortex (assessment of perfusion and glucose metabolism using PET) can be a method to confirm the disease. Determination of biomarkers in cerebrospinal fluid (CSF) makes it possible to identify pre-existing asthma in both preclinical and early clinical stages. Biomarkers are compounds found in a certain pathology; their presence confirms the diagnosis. For AD, these are beta-amyloid and tau protein. Normally, beta-amyloid can also be present in the CSF, and its concentration in healthy people is higher than in patients with AD - with the development of AD, amyloid protein accumulates in brain tissue, and its concentration in the CSF decreases. These changes are combined with an increase in the level of tau protein and the appearance of its special form - hyperphosphorylated tau protein. The concentration of tau protein in the CSF increases with the death of neurons in cerebral structures, for example, during stroke, encephalitis, generalized epileptic seizure, etc. Hyperphosphorylated tau protein is considered a specific compound for AD. Thus, the disease can be established by a simultaneous decrease in the level of amyloid protein and an increase in the level of tau protein in the CSF in combination with the appearance of hyperphosphorylated forms of tau protein. In some cases, especially in familial forms of AD, genetic testing may be useful.

Modern ideas about the diagnosis of asthma are reflected in new “research” criteria for this disease. Research criteria for the diagnosis of AD (according to B. Dubois et al.):

memory impairment, which is characterized by: [ 1 ] gradual progression (at least 6 months), according to the testimony of the patient or his relatives; [ 2 ] objective impairments of episodic memory according to neuropsychological testing (memory impairments are not corrected by prompts during reproduction or by providing multiple choice); [ 3 ] disorders of episodic memory, which are isolated or combined with other cognitive disorders;

one of the following signs: [ 1 ] atrophy of the medial temporal lobe according to neuroimaging data; [ 2 ] AD-specific changes in the CSF (decreased content of amyloid oligomers, increased content of tau protein); [ 3 ] hypometabolism of the temporoparietal regions or cerebral amyloidosis according to PET data.

UPDATED CRITERIA FOR BA DIAGNOSIS

Experts from the NIA (National Institute on Aging) have identified three stages of AD:

[1 ] asymptomatic preclinical- the use of biomarkers is the main diagnostic method (see table); these changes may fit into the category of “mild cognitive impairment”; In addition, it is proposed to diagnose the same preclinical stage in individuals who carry a pathological isoform of the apoE gene, as well as in carriers of autosomal dominant mutations. B. Dubois et al. proposed to distinguish asymptomatic individuals (patients with the presence of biomarkers of Alzheimer's pathology, who may not develop the clinical stage, who are at risk of developing AD) and preclinical AD (individuals who carry autosomal dominant mutations, which implies mandatory further progression of the disease);

read also the post: Alzheimer's syndrome(to the site)

[2 ] pre-dementia - corresponds to moderate cognitive impairment (MCI); criteria for diagnosing MCI as a predementia stage of AD have been developed in two versions - using only clinical signs and with additional determination of biomarkers (see table);

[3 ] dementia (see table).

Treatment. Treatment of asthma should be carried out comprehensively using different drugs, the action of which is aimed at the most important mechanisms of disease development. The main directions of treatment: compensatory, i.e. replacement therapy (based on replenishing neurotransmitter deficiency in various mediator systems: cholinergic, glutamatergic, serotonergic), neuroprotective therapy, psychopharmacotherapy of productive mental disorders, psychological correction, patient care. Basic symptomatic therapy for asthma includes two classes of drugs: [ 1 ] central acetylcholinesterase inhibitors (ACHES-I), the most effective and frequently used among them are rivastigmine, galantamine, donepezil; [ 2 ] N-methyl D-aspartate (NMDA) receptor antagonist - memantine hydrochloride (akatinol memantine). The beneficial effects of these drugs in mild to moderate dementia are well known. Unfortunately, for most drugs from the group of nootropic therapy there are no results of double-blind, randomized, placebo-controlled studies proving their effectiveness, which does not meet modern standards for assessing the pharmacoeffectiveness of drugs. Due to the mandatory availability of the necessary evidence base for recommending a drug for use, Cerebrolysin should be noted. Clinical studies performed in accordance with the required standards have shown the effectiveness of its use as an additional symptomatic remedy for asthma. Non-drug methods for treating cognitive impairment include: diet, cognitive-motor training, psychological and behavioral correction methods, psychotherapeutic approaches, meditation and yoga. Physical activity and exercise also have a positive effect on cognitive function. Frequently used methods include aerobic exercise, resistance exercise, stretching, strength and balance training, and dual-task training. Preference is given to aerobic training.

about non-pharmacological approaches in the treatment of asthma read the article “Alzheimer's disease: pharmacological and non-pharmacological approaches to the correction of psychoneurological disorders” Mendelevich E.G.; Department of Neurology and Rehabilitation of the Federal State Budgetary Educational Institution of Higher Education "Kazan State Medical University", Kazan, Republic of Tatarstan (magazine "Neurology, neuropsychiatry, psychosomatics" No. 3, 2018) [read]

Read more about BA in the following sources:

article “Alzheimer's disease” Koberskaya N.N.; Federal State Autonomous Educational Institution of Higher Education “First Moscow State Medical University named after. THEM. Sechenov" Ministry of Health of the Russian Federation, Moscow (journal "Neurology, neuropsychiatry, psychosomatics" 2019, Appendix 3) [read];

article “Current aspects of diagnosis and treatment of Alzheimer's disease (based on modern foreign recommendations)” by M.V. Nesterova, Ural State Medical University (magazine “Medical Council” No. 6, 2018) [read];

article “A new look at the pathogenesis of Alzheimer’s disease: modern ideas about amyloid clearance” Lobzin V.Yu., Kolmakova K.A., Emelin A.Yu.; Military Medical Academy named after S.M. Kirova, St. Petersburg (magazine “Review of Psychiatry and Medical Psychology” No. 2, 2018) [read];

article “Management of patients with Alzheimer’s disease” by V.A. Parfenov, A.R. Kabaeva; First Moscow State Medical University named after. THEM. Sechenov Ministry of Health of Russia (magazine “Medical Council”, No. 1, 2018) [read];

article “Alzheimer's disease: new diagnostic criteria and therapeutic aspects depending on the stage of the disease” N.N. Koberskaya, First Moscow State University named after. THEM. Sechenov Ministry of Health of Russia (magazine “Medical Council” No. 10, 2017) [read];

article “Neuroimaging methods for diagnosing Alzheimer's disease and cerebrovascular diseases accompanied by cognitive impairment” Litvinenko I.V., Emelin A.Yu., Lobzin V.Yu., Kolmakova K.A.; Federal State Budgetary Educational Institution of Higher Education "Military Medical Academy named after. CM. Kirov" Ministry of Defense of the Russian Federation, St. Petersburg (journal "Neurology, neuropsychiatry, psychosomatics" 2019, Appendix 3) [read];

article “Extrapyramidal disorders in Alzheimer's disease: implications for differential diagnosis and patient management” Zakharov V.V., Kabaeva A.R.; Federal State Autonomous Educational Institution of Higher Education “First Moscow State Medical University named after. THEM. Sechenov" Ministry of Health of the Russian Federation, Moscow (Neurological journal, No. 4, 2017) [read];

article “Early diagnosis and therapy of Alzheimer’s disease” by N.N. Koberskaya, First Moscow State Medical University named after. THEM. Sechenov (magazine “Effective Pharmacotherapy” No. 31, 2017 [read]);

article “Modern ideas about the pathogenesis of Alzheimer’s disease: new approaches to pharmacotherapy (review)” by Yu.K. Komleva, N.V. Kuvacheva, O.L. Lopatina, Ya.V. Gorina, O.V. Frolova, E.A. Teplyashina, M.M. Petrova, A.B. Salmina; Krasnoyarsk State Medical University named after. Professor V.F. Voino-Yasenetsky (magazine “Modern Technologies in Medicine” No. 3, 2015) [read];

article “Beta-amyloid and Tau protein: structure, interaction and prion-like properties” by O. G. Tatarnikova, M. A. Orlov, N. V. Bobkova; Institute of Cell Biophysics RAS, Moscow region, Pushchino; Pushchino State Natural Science Institute, Moscow region, Pushchino (journal “Advances in Biological Chemistry” vol. 55, 2015) [read];

article “Some genetic aspects of the development and treatment of Alzheimer’s disease” Preobrazhenskaya I.S., Snitskaya N.S.; State Budgetary Educational Institution of Higher Professional Education “First Moscow State Medical University named after. THEM. Sechenov”, Moscow, Russia (magazine “Neurology, neuropsychiatry, psychosomatics” No. 4, 2014) [read];

article “Preclinical stage of Alzheimer's disease (Review of foreign literature)” by A.G. Vlasenko, D.K. Morris, M.A. Minton, S.N. Illarioshkin; Department of Radiology, Washington University School of Medicine, St. Louis, USA; Alzheimer's Disease Research Center, Department of Neurology, Washington University School of Medicine, St. Louis, USA; Radiopharmaceutical company Avid Radiopharmaceuticals, Philadelphia, USA; Scientific Center for Neurology of the Russian Academy of Medical Sciences, Moscow (Neurological Journal, No. 2, 2012) [read];

article “New criteria for diagnosing Alzheimer’s disease” by A.Yu. Emelin; Department of Nervous Diseases of the Military Medical Academy named after. CM. Kirova, St. Petersburg (magazine “Neurology, neuropsychiatry, psychosomatics” No. 4, 2011) [read];

article “Diagnosis and treatment of Alzheimer’s disease” Naumenko A.A., Gromova D.O., Trofimova N.V., Preobrazhenskaya I.S.; Department of Nervous Diseases and Neurosurgery of the Federal State Budgetary Educational Institution of Higher Education “First Moscow State Medical University named after. THEM. Sechenov" of the Ministry of Health of Russia, Moscow (magazine "Neurology, neuropsychiatry, psychosomatics" No. 4, 2016) [read];

article “Treatment of Alzheimer's disease” by Tyuvin N.A., Balabanova V.V.; Department of Psychiatry and Narcology, State Budgetary Educational Institution of Higher Professional Education “First Moscow State Medical University named after. THEM. Sechenov" of the Ministry of Health of Russia, Moscow (magazine "Neurology, neuropsychiatry, psychosomatics" No. 3, 2015) [read];

article “Treatment of cognitive deficits in Alzheimer's disease” [review of the article by C. Campos et al. “Treatment of Cognitive Deficits in Alzheimer's disease: A psychopharmacological review”, published in the journal Psychiatria Danubina (2016; Vol. 28, No. 1;2-13), which describes the effectiveness of cholinesterase inhibitors (ChEIs) and N-methyl-receptor agonists D-aspartate (NMDA) in the treatment of cognitive impairment in Alzheimer's disease] (prepared by Larisa Kalashnik; Neuronews magazine No. 10(84), 2016) [read];

article “New methods of treating Alzheimer's disease, currently in clinical trials” by K.P. Skibin; Kharkov National Medical University (2013) [read];

article “Modern approaches to therapy for Alzheimer’s disease: from amyloid to the search for new targets” by D.I. Rodin, A.L. Shvartsman, S.V. Sarantseva; National Research Center "Kurchatov Institute" of the St. Petersburg Institute of Nuclear Physics named after B. P. Konstantinov; Institute of Experimental Medicine, St. Petersburg (Scientific notes of St. Petersburg State Medical University named after academician I.P. Pavlov, T. XXI, No. 1, 2014) [read];

article “Prevention of Alzheimer's disease” by V.A. Parfenov; Department of Nervous Diseases, State Budgetary Educational Institution of Higher Professional Education “First Moscow State Medical University named after. THEM. Sechenov" of the Ministry of Health of Russia, Moscow (magazine "Neurology, neuropsychiatry, psychosomatics" No. 3, 2011) [read];

project “Federal Clinical Guidelines for the Diagnosis and Treatment of Alzheimer’s Disease” Ministry of Health and Social Development of the Russian Federation, Federal State Budgetary Institution “Scientific Center for Mental Health” of the Russian Academy of Medical Sciences (2013) [read];

manual for doctors “Dementia” N.N. Yakhno, V.V. Zakharov, A.B. Lokshina, N.N. Koberskaya, E.A. Mkhitaryan (3rd ed., Moscow, “MEDpress-inform” 2011, pp. 53 - 75) [read];

article “Pharmacotherapy and dementia” by M.Yu. Drobizhev, A.V. Fedotova, S.V. Kikta, E.Yu. Antokhin, Federal State Budgetary Educational Institution of Higher Education “First Moscow State Medical University named after. THEM. Sechenov", Moscow, Russia; Federal State Budgetary Educational Institution of Higher Education "Russian National Research Medical University named after. N.I. Pirogov”, Moscow, Russia; Federal State Budgetary Institution "Polyclinic No. 3" of the Medical Center of the Administration of the President of the Russian Federation, Moscow, Russia; State Budgetary Educational Institution of Higher Professional Education "Orenburg State Medical University" Ministry of Health of the Russian Federation, Orenburg, Russia (Journal of Neurology and Psychiatry, No. 10, 2016) [read]

© Laesus De Liro

Treatment of psychiatric symptoms

The main treatable neuropsychiatric disorders in Alzheimer's disease are:

Agitation

Depression

• Anxiety states

  Sleep disturbance (insomnia)

Symptoms in patients with Alzheimer's disease can be treated with antipsychotics, antidepressants, anticonvulsants, and other psychopharmacological agents (medicines used to treat psychiatric disorders). The target symptoms must be clearly defined and documented. Treatment should be under constant supervision and regular monitoring of effectiveness.

Agitation occurs in 70% of patients with Alzheimer's disease and mainly as the disease progresses. Psychopharmacologic agents used to treat agitation include the following classes: antipsychotics, anticonvulsants, mood-stabilizing drugs such as trazadone, anxiolytics, and beta-blockers. Available evidence supports that antipsychotics such as trazadone or anticonvulsants are effective in treating agitation. Atypical antipsychotic agents such as clozapine, risperidone, olanzapine, quetiapine, and ziprasidone have advantages over previously used antipsychotic agents based on side effects and the patient's ability to tolerate them.

Psychoses Quite common among Alzheimer's patients, approximately 50% of cases. Atypical antipsychotics are the treatment of choice. Risperidone and olanzapine have benefits, but quetiapine and ziprasidone may also provide benefit. Sedation (weakness, calmness) is the most common side effect observed in patients taking antipsychotics.

Symptoms depression often occur in patients suffering from Alzheimer's disease, in approximately 50% of patients. But major depression is a more unusual phenomenon. Treatment for symptoms of depression usually consists of selective serotonin reuptake inhibitors (SSRIs) such as sertraline, citalopram or fluoxetine. Full doses of SSRIs are generally well tolerated by older adults, unlike most other psychotropic agents, which are usually prescribed in low doses. As an alternative, tricyclic antidepressants can be used in combination with some anticholinergic drugs (side effects - dry mouth, constipation, memory impairment), for example, nortriptyline or a combination drug of norepinephrine and serotonin reuptake inhibitors, for example, venlafaxine.

Anxious state It is also quite common in people suffering from Alzheimer's disease. In 40%-50% of cases, patients experience anxiety at some point during the course of the disease. Most patients with anxiety do not require medication. For those who require drug treatment, it is best to avoid benzodiazepine treatment due to the possible negative effects on thinking. Treatment is preferable with non-benzodiazepine anxiolytics such as buspirone or SSRIs.

Sleep disturbance (insomnia) occurs in many patients with Alzheimer's disease at some point during the course of the disease. Agents used in the treatment of insomnia in patients with Alzheimer's disease are mild short-acting benzodiazepines such as Temazepam, non-benzodiazepine sedative hypnotics such as Zolpidem or Zaleplon, or sedating antidepressants such as Trazadone. Measures to improve sleep should also be taken, such as exposure to sunlight, adequate pain management, and limited fluid intake at night.