Background: much research has been devoted to investigation of pathological grief reaction (PGR) in late age and its affective disorder outcomes, however the role of PGR in the development of dementia in the elderly and old age patients is studied insufciently. The aim of the study was to investigate the PGR role in the development of dementia in late age and to determine the impact of psyсhogenic experience on the course and specifcities of the clinical picture in Alzheimer’s disease (AD) and vascular dementia (VaD). Material: during continuous examination of 134 patients, frst hospitalized in geriatric departments of MHRC clinic due to dementia, 42 subjects were selected (31,3% from the total number of hospitalized patients), having endured bereavement of emotionally important person in late age. Two groups were formed from among of these patients: the main group, consisting of 20 patients (46,7% from the patients of general sample), having endured bereavement of important person with PGR, and comparison group, including22 patients (53,3%), in whom bereavement was not accompanied with PGR. Two groups of patients with dementia syndrome in AD and VaD were comparable according to various clinical and demographic parameters. Methods were used as follows: psychopathological, clinical, brain MRI, psychometric (MMSE), neuropsychological examination. Results: the study showed, that in patients with PGR in the past medical history terms of development of marked manifestations of dementia syndrome reduced almost twice, and in the structure of the main disease reactive experiences were preserved in the form of PRG symptoms although in an erased state. Residual PRG symptoms in the structure of dementia have defnite specifc character depending on nosological belonging of dementia. In AD psychopathological disorders presented more often the form of delusions and perception illusion, and in VaD the symptoms bear more marked affective character. Conclusion: PGR in aged may be a trigger of manifestation, or quick increase of dementia. The clinical picture of dementia is complicated by residual PGR symptoms. The risk of dementia manifestation following the development of pathological grief reaction makes it necessary to carefully study cognitive functions in individuals, enduring bereavement in old age, and timely beginning of anti dementia treatment.

Aim: to compare distributions of glutamine synthetase (GS) and glutamate dehydrogenase (GDH) activities and amounts of their immunoreactive forms amongst frontal, anterior, posterior cingulate, and cerebellar cortices in schizophrenia cases and controls. Material and methods: group of patients with schizophrenia: 4 men and 4 women (36–80 years old) diagnosed according ICD-10 (F20.00, F20.02, F20.31, and F20.50 — 3, 3, 1 and 1 patient). Control group: 8 men and 1 woman (29–79 years old). No significant between-group differences were found in age and postmortem interval (p > 0,05). Non-parametric statistics was used. Results: no signifcant between-group difference was observed in GS activity in investigated brain structures (p > 0,05). Following differences were found in schizophrenia compared with controls: amount of immunoreactive GS was decreased in frontal cortex (p < 0,001), it was increased in posterior cingulate cortex and cerebellum (p < 0,001 and p < 0,004), but unchanged in anterior cingulate cortex, whereas level of GS-like protein (GSLP) was signifcantly elevated in all four brain structures (р < 0,004, р < 0,02, р < 0,04, and р < 0,001). When compared with controls, schizophrenia cases displayed elevated GDH activity in frontal, posterior cingulate cortex and cerebellum (p < 0,004, p < 0,05, and p < 0,002), but unchanged in anterior cingulate cortex. When compared with control, following differences were found in schizophrenia: elevation in levels of immunoreactive GDHI, GDHII, and GDHIII in frontal cortex (р < 0,008, р < 0,003, and р < 0,001); elevation in levels of immunoreactive GDHI, GDHII, and GDHIII in posterior cingulate cortex (р < 0,004, р < 0,001, and р < 0,02); elevation in levels of immunoreactive GDHII and GDHIII in cerebellum (р < 0,02 and р < 0,001). No between-group differences in levels of immunoreactive GDH forms were found in anterior cingulate cortex. Conclusion: alteration in levels of GS, GSLP, and GDH forms in brain of patients with schizophrenia is one of causes of glutamate metabolism disturbances in these brain structures and an important aspect of schizophrenia pathogenesis.

Aim of the study: investigation of dynamic features of endogenous affective disorders occurring with apathetic depressions, revealing common patterns and differences in mono- and bipolar patients, investigation of prognosis features in two groups. Material: 25 patients (12 male, 13 female) suffering from endogenous apathetic depression were included (13 with recurrent depressive disorder and 12 with bipolar affective disorder). Methods: psychopathological and catamnestic methods were used (follow-up period up to 7 years). Results and conclusion: study results provided information about common dynamic patterns in endogenous affective disorders, and differences concerning frequency and development mechanism of affective phases, duration and intensity of manifest and recurrent affective states, intensity of depressions, quality of remissions and other features. In case of recurrent depressive disorder there was detected less frequency and intensity of affective states, but greater duration of depressions as compared with bipolar affective disorder, therefore life quality prognosis in two groups was evaluated as equal.

The aim of the study was to investigate the clinical-pathological specifcities of psychopathy like depressions with hysterical disorders, to develop their typology, to study regularities of their dynamics, to reveal special features of their clinical picture in a case of various endogenous diseases, and to develop optimal therapeutic approaches. Patients. A total of 55 patients (45 females and 10 males) aged 18–55 were included in the study. Inclusion criterion was the presence of depressive state with a predominance of hysterical psychopathy like symptomatology. Methods: clinical-psychopathological; clinical and follow-up methods. Results and conclusion: the analysis of psychopathological structure of endogenous depressions with hysteroform psychopathy like disorders detected their clinical polymorphism. Different symptoms of conversion-dissociative symptomocomplex vary from simple sensory, motor, and sensible conversions in the structure of hystero-hypichondriac depression to pathogenetically integral conversion and mental (dissociative) impairments in hystero-psychotic depressions. The predominance of anxiety and apathetic hypothymic radical allows classifying of psychopathy like hysteroform depressions as anxiety-apathetic ones. The following three phenomenologically different anxiety variants were singled out: cothymia (combination of endogenous, predominantly paroxysmal, and neurotic anxiety) in a case of hystero-hypochondriac depressions; 2) endogenous anxiety in combination with motor agitation within the framework of affective-mixed state in hystero-behavioral depressions; 3) endogenous anxiety with projection to external stimuli in hystero-psychotic depressions.

Background: it is assumed that a number of metabolic changes and initial psychopathological anomalies of patients with endogenous psychoses are formed long before the manifestation of the disease, is associated with a hereditary, genetic component and can be reflected in the constitutional features of the patients already in the premorbid period of the disease and be a promising method for early recognition. Previously, the participation of PPARGC1A (Peroxisome proliferator-activated receptor gamma coactivator 1-alpha) and AGTR1(Angiotensin II Receptor Type 1) genes in the formation of both metabolic and morphofunctional, neurodegenerative, cognitive and other mental disorders was repeatedly demonstrated. The aim of study was to study the frequency distribution of the polymorphic markers G1444A of the PPARGC1A gene (rs8192678) and A1166C of the AGTR1 gene (rs5186) in patients with schizophrenia (ICD-10: F20, F25), depending on their afliation to the subgroups isolated according to the severity of premorbid personality anomalies: accentuated, with personality disorder (or psychopathy), with pseudopsychopathy. Material: a sample of patients was formed of in-patients (all men) of clinical unit of FSBSI «Mental health research centre». The control group consisted of 290 healthy men. DNA for the study was isolated from the venous blood of the recipients. Methods: genotyping was performed by standard PCR with further analysis of MspI restriction fragments (for rs8192678) and DstDEI fragments (for rs5186). Statistical processing of data was carried out using the program Statistica 6.0. Results: the association of studied markers with the severity of premorbid personality anomalies in patients was revealed. Thus, in the subgroup of patients with personality disorder, an increase in the frequency of the CC genotype (A1166C of the AGTR1 gene) and a decrease in the frequency of the GG genotype (G1444A of the PPARGC1A gene) compared to other subgroups; and in the subgroup of patients with pseudopsychopathy — a decrease in the frequency of the genotype CC (A1166C gene AGTR1) and an increase in the frequency of the genotype GG (G1444A gene PPARGS1A). This may indicate the possible involvement of these genes in the formation of psychopathological and biological changes in patients with schizophrenia at the stages preceding the manifestation of the disease.

Postpartum depression is an prominent problem of women’s mental health due to the high prevalence and substantial negative impact on the formation of mother–child communication and the well-being of the newborn. Nevertheless, the aspects of psychopathology, dynamics and nosology of postpartum depressions remain unspecifed. This publication is devoted to a critical analysis of the current state of the problem of postpartum depression of the current state of the problem of postpartum depression on the basis of the recently published article «Postpartum Depressions: Clinico-psychopathological Aspects and Typology» by L.V. Vasyuk, literature data and the results of our own research.

Background. Diabetes mellitus is one of the most frequent chronic diseases, affecting up to 10% of the population. The risk of dementia in patients with diabetes increases by an average of 1,6 times, with the risk of vascular dementia 2–2,6 times, and the risk of Alzheimer’s disease (AD) — about 1,5 times, regardless of age diabetes onset. The aim was to review scientifc publications on the role of hyperglycemia in the development of cognitive dysfunction. Results: on shown that only a moderate, predominantly neurodynamic cognitive defcit can be associated with it. Apparently cerebrovascular or neurodegenerative pathology, accelerated by metabolic disorders in diabetes, and hypoglycemic episodes, can play a more important role in the development of cognitive decline. A parallelism in the development of diabetes and AD is largely explained by insulin dysfunction. The decrease with age of insulin concentration and the number of insulin receptors in the brain partially explains the age-related cognitive dysfunction. Therapy, simultaneously directed to several key pathophysiological links in the development of diabetic encephalopathy, appears to be the most promising. It can include a combination of drugs acting on different therapeutic targets, or those few multicomponent drugs that can directly affect several targets. Conclusion: current conceptions of diabetes pathogenesis determine complex therapeutical intervention.

The aim of work was to present the analysis of current scientifc publications devoted to the problem of frontotemporal dementia. Material and methods: according to the key words «frontotemporal dementia» and «frontotemporal lobar degeneration» publications over the last two decades were chosen and analyzed in PubMed, MEDLINE, and other scientifc bases. Results: at present the phenomenology and diagnostic criteria of the basic types of frontotemporal dementia (FTD) are presented in the literature in the most developed form. The progress in recognition of the disease and its separate types is based on the results of investigation of modern neuroimaging methods diagnostic signifcance. FTD is considered to be one of the leading reasons for early onset of dementia, however, the prevalence of FTD in the population of senior age groups has been studied insufciently. Achievements of molecular-genetic FTD studies determine directions of further research of the pathogeny of the disease and perfection of its systematics. Prospectivity of investigation of separate risk factors and their combinations as an important task of further clinical and population studies was substantiated. The results of symptomatic therapy with application of memantin for the treatment of dementia as well as SSRI for correction of behavioral disorders were considered. Conclusion: the perfection of FTD systematics and the achievements of neurosciences create the prospects of the development of effective methods of symptomatic pharmacotherapy (memantin, SSRI) and nosomodifcating therapeutic intervention with application of gene technologies.

The conceptualization of negative symptoms has evolved in recent years; it is largely recognized that negative symptoms may be primary (related to the disease process) or secondary to other factors (i.e. positive symptoms, depression, side effects of drug treatment) and cluster in two dimensions: avolition (including amotivation, anhedonia and asociality) and defcit of expression (including affective flattening and alogia) that might have a different impact on functional outcome.

Alzheimer’s disease is a common neurodegenerative disease characterized by memory impairment and a progressive incurable cognitive decline. Modeling Alzheimer’s disease in animals allows to study the pathogenesis of the disease, to conduct preclinical studies, to search for possible ways to stop the development and progression of the disease. Since the etiology of Alzheimer’s disease remains unknown, there is no «natural» biological model that fully reflects the set of pathological disorders that occur in a person with this pathology, and among a variety of options of pathogenetic models there is no generally accepted one. This review provides an analysis of data on modern approaches to modeling Alzheimer’s disease in animals. The important aspects to be taken into account in modeling (metabolic disorders of β-amyloid and tau protein, the role of inflammatory reactions, etc.) have been analyzed. We review such widespread models as the use of transgenic animals of the frst and second generations expressing human genes with mutations found in the family form of the disease; models of natural aging and senescence-accelerated animals; intraventricular neurotoxin injection models. We also discuss more rare surgical models that phenotypically simulate some aspects of Alzheimer’s disease. An important role of inflammatory reactions in the pathogenesis of the disease is analyzed, which causes interest in models of neuroinflammation that manifests itself before the development of other pathological disorders characteristic for Alzheimer’s disease. We assess the advantages and limitations of each model, the features of their application, the main results obtained with their help, promising directions for further researches.

The 1 part deals with the review of current foreign and domestic views on the etiology, neurochemistry, and pathophysiology of anxiety-depressive disorders. Theories of emergence, neuromediator systems, and anatomic structures, engaged in the pathogenesis of anxiety-depressive disorders, were discussed. On this basis current trends of pathogenetic therapy of anxiety will be presented in the second part.

The aim was to create a logical connection between neurobiological models, experimental data and the clinical use of SSRIs to the treatment of anxiety and depressive disorders. Method: a systematic review and an analyzis of scientifc publications. Results: data of clinical investigations give a presentation on mechanisms of action, clinical aspects and side effects of SSRI antidepressants. Attention has been paid to the interpretation of the various behaviors, associated with these disorders through the prism of experimental neurobiology. Particular attention is paid to the neurobiological basis of the clinical and side effects of serotonin reuptake group antidepressants. There are background recommendations to use receptor profles of SSRIs for good clinical therapeutic results. Conclusion: this knowledge would be used in routine clinical practice.