Репозиторий Университета

© 2018 ABV-Press Publishing House. All rights reserved. Background. Patients with the chronic migraine frequently present with memory and attention complaints. However, the prevalence and phenotype of such impairment in chronic migraine have not been studied. Objective-to evaluate the prevalence of the objective cognitive deficit in patients with chronic migraine and factors underlying its etiology. Materials and methods. We recruited 62 subjects with chronic migraine and 36 gender-and age-matched controls with low-frequency episodic migraine (not more, then 4 headache days per month) aged 18-59. All patients filled in the Hospital Anxiety and Depres sion Scale (HADS) and Sheehan Disability Scale. Cognitive function was assessed with the Montreal Cognitive Assessment (MoCA), Digital Symbol Substitution Test (DSST), Rey Auditory Verbal Learning Test (RAVLT), and the Perceived Deficits Questionnaire (PDQ-20). Results. In this study 58 % of patients with chronic migraine complained of memory loss. Cognitive impairment was also found with PDQ-20. Objectively, we found a significant decrease in 90-second DSST results and RAVLT total recall and learning rate. In 40 % of subjects with chronic migraine scored lower than 26 points on MoCA. Patients with chronic migraine more frequently had lower DSST rates as compared to episodic migraine (odds ratio 5.07 (95 % confidence interval-1.59-16.17); p = 0.003). Depression and anxiety did not correlate with performance on cognitive tests. Chronic migraine (frequent headache) and longer headache history, but not depression, anxiety or medication overuse were independent predictors of cognitive impairment. Conclusion. Subjective and objective cognitive deficits are prevalent in the chronic migraine population. Most often memory and attention are impaired. Longer headache history and presence of chronic migraine are independent risk factors for cognitive impairment in patients with chronic migraine.

© 2018 Ima-Press Publishing House. All Rights Reserved. This review provides information on prospects for using the antidepressant agomelatine in neurological practice. The drug has a unique receptor profile, being a melatonin receptor type 1 and 2 agonist and a serotonin receptor subtype 2C antagonist. Due to this and in addition to antidepressant action, the drug has a number of other effects, such as analgesic, anti-apathetic, anti-asthenic, procognitive, anxiolytic, and sleep-normalizing ones, which are of great importance in the treatment of neurological diseases. There are clinical and experimental data that prove the high efficiency and safety of agomelatin in the follow-up of patients with post-stroke depression, Parkinson's disease, Alzheimer's disease, Pick's disease, Huntington's disease, chronic fatigue syndrome, and pain syndromes.

© 2018, Media Sphera Publishing Group. All rights reserved. Objective. To study cognitive functions, anxiety and depression levels, 24-hour blood pressure (BP) profile, cerebral blood flow (CBF) perfusion in treatment-naive middle-aged patients with uncomplicated essential arterial hypertension (EAH) depending on the white matter hyperintensities (WMH) burden. Material and methods. Forty-one hypertensive patients (mean age 46.2±4.6 years) and 41 healthy volunteers (mean age 50.3±6.7 years) were enrolled to the study. All subjects underwent brain MRI (MAGNETOM Skyra 3.0T, T1, T2 FSE, T2 FLAIR, T1 MPRAGE, ASL), Montreal cognitive assessment (MoCA), 10-word learning task, verbal fluency test, trail making test, Stroop color and word test, anxiety and depression assessment with Hamilton rating scales, 24-hour blood pressure monitoring (ABPM). Results. WMH were found in 22 (53.7%) hypertensive patients and in 3 (7.3%) healthy volunteers (p=0.0002). Hypertensive patients had the significantly lower CBF compared to controls (p<0.001). Conclusion. WMH were identified in treatment-naive middle-aged patients with uncomplicated mild to moderate EAH. There was an association between WMH and lower CBF in the cortical plate of frontal lobes, SBP variability and worse cognition. Cerebral hypoperfusion can cause cognitive impairment even in the earliest stages of EAH, which increases due to emotional disorders.

© ABV-Press Publishing House. All rights reserved. Over a half of chronic pain (CP) patients present with cognitive complaints, which increase their disability and impact quality of life. The paper reviews objective impairments in memory, attention, processing speed and executive function demonstrated in the CP population. The paper also reviews common pathology underlying cognitive impairment and CP: neuroplasticity in the shared brain areas, neurotransmitter and other molecular mechanisms. Common mechanisms in CP and depression precipitating cognitive impairment are also discussed. The paper also compares the potential of different antidepressants to improve cognitive functions in depression and CP.

© 2018, Media Sphera Publishing Group. All rights reserved. Non-motor disturbances represented by sensory, affective, obsessive-compulsive disorders, cognitive dysfunction, sleep disturbances are often found in patients with dystonia and have a negative impact on their quality of life. The prevalence of sensory and affective disorders and sleep disturbances is above 50% in patients with cervical dystonia and is 25% in patients with blepharospasm, writing spasm; cognitive dysfunction is found in more than 25% of patients with focal dystonia. The relationship of nonmotor, in particular psychiatric disorders, with the impairment of social and everyday life and worsening of quality of life in whole was shown. Common pathophysiological mechanisms of non-motor disorders as well as approaches to treatment of these disorders are discussed. The authors present the results on the positive effect of botulinum toxin therapy that reduces cognitive dysfunction, sensory disorders and depressive syndrome. Non-medication treatment of non-motor disorders in patients with dystonia is considered.

© 2018 Media Sphera Publishing Group.All Rights Reserved. Aim. To evaluate the presence and the severity of the complaints (headache, dizziness, memory loss, concentration of attention, sleep disturbances, decreased mood, increased anxiety), the state of cognitive functions, emotional status and quality of night sleep in treatmentnaïve middle-aged patients with mild to moderate EAH compared to healthy volunteers of the same age. Materials and methods. 103 treatment-naïve patients with EAH aged 40-59 years at the enrollment, who met the inclusion/exclusion criteria and provided written informed consent (46 men, mean age 53.6±0.8 years) and 50 healthy volunteers (17 men, mean age 51.5±1.0 years) with normal blood pressure (BP) level - control group - were enrolled to the study. Mean EAH duration was 2.9±5.7 years. Cognitive assessment included Montreal cognitive assessment, 10-words learning task, verbal fluency test, TMT, Stroop color and word test. Anxiety and depression were evaluated via Hamilton rating scales (HARS and HDRS). 24-hours ambulatory BP monitoring (ABPM) was performed according to European guidelines. Results. 70% of patients with EAH complained of memory disturbance, 68% - lack of attention, 22% - sleep disturbances, 12% - dizziness, 9% - headache. It took statistically significant more time for patients with EAH to perform on TMT B (p<0.05), they had significantly higher TMT B - TMT A difference score (p<0.01) and lower mean MoCA score (p<0.05). Patients with EAH had significantly higher mean score in Hamilton anxiety (2.1±3.7) and depression (1.1±2.4) rating scales compared to controls (0.3±0.9 points, p<0.01 and 0.1±0.5 points, p<0.001, respectively). Patients with EAH who complained of sleep disturbances had low sleep quality (8.7±2.8 points). Among patients with EAH who complained about headaches 66.6% had episodic migraine and chronic tension type headache (33.4%). Those patients had a substantial impact of headache on life and daily living according to HIT-6 (mean score - 57.5±6.1). Only 2 patients out of 12 with complains about dizziness had benign paroxysmal positional vertigo and Ménière's disease. Conclusion. Complaints about memory dysfunction, lack of attention, sleep disturbances, less common - dizziness and headaches, are most typical in patients with EAH on the early stages of the disease. They differ from healthy volunteers of the same age by having cognitive impairment and higher anxiety and depression scores. Patients with EAH who complained about sleep disturbances had low sleep quality. Headache in patients with EAH was due to episodic migraine and tension type headache which had a negative impact on life and daily living.

© 2018 ABV-Press Publishing House. All rights reserved. Background. Memory and attention deficits are prevalent in the chronic pain population. There are multiple common mechanisms in chronic pain and cognitive impairment. However, the presence, prevalence and clinical burden of such impairment are frequently underestimated. Objective: to evaluate subjective and objective cognitive deficits in patients with chronic migraine (CM). Materials and methods. We recruited 53 subjects with CM and 22 gender- and age-matched controls with low-frequency episodic migraine (a maximum of 4 headache days per month) aged 18-59. All patients filled in the HADS (Hospital Anxiety and Depression Scale) anxiety and depression scale and Pittsburg Sleep Quality Inventory (PSQI). Cognitive function was assessed with Montreal Cognitive Assessment (MoCA), Digital Symbol Substitution Test (DSST), Rey Auditory Verbal Learning Test (RAVLT) and the Perceived Deficits Questionnaire (PDQ-20). Results. 56 % of patients with CM complained of memory problems. Decreased cognitive function was also observed during self-assessment using the PDQ-20 questionnaire. Objectively, we found a significant decrease in 90-second DSST results and RAVLT total recall and learn ing rates. 44 % of subjects with CM scored lower than 26 points on MoCA. Most frequently we found impairments in attention (75 %), memory/delayed recall (50 %), language (50 %) and executive function (37 %). Depression and sleep quality correlated with only several parameters of cognitive tests. Conclusion. Subjective and objective cognitive deficits are prevalent in the CM population. Most often memory and attention are impaired. Cognitive complaints need to be carefully assessed, and treatment of such impairment may improve quality of life and decrease disability in CM.

© 2018 Ima-Press Publishing House. All rights reserved. Objective: to determine the main factors associated with the development and manifestations of anxiety and depression spectrum disorders (ADSDs) in patients with Behcet’s disease (BD). Subjects and methods. This investigation was conducted within the framework of the interdisciplinary scientific program «Stress factors and mental disorders in rheumatic diseases». A total of 116 patients with BD were examined. Most of them were men (69.8%), whose mean age (M±σ) was 33.4±9.82 years; the median duration of BD was 120.0 [70.0; 192.0] months; 51.9% of the patients were natives of the North Caucasus. All the patients had a reliable diagnosis of BD according to the International Study Group for Behcet’s disease (ISGBD) criteria (1990). Disease activity was assessed using the Behcet’s Disease Current Activity Form (BDCAF); the subjective status of patients was evaluated using the visual analog scale (VAS) for general health assessment. ADSDs were diagnosed by a psychiatrist according to the ICD-10 during semi-structured interviews using the Hospital Anxiety and Depression Scale (HADS), the Hamilton Anxiety Rating Scale (HAM-A), and the Montgomery-Asberg Depression Rating Scale (MADRS). Clinical and psychological techniques were applied to assess cognitive functions (memory, attention, and logical thinking); stress levels were estimated by the 10-Item Perceived Stress Scale (PSS-10). Results and discussion. ADSDs were diagnosed in 91 (78.4%) patients with BD. The predominant RTDs were dys-thymia (39.6%) and recurrent depressive disorder (38.4%). Generalized anxiety disorder was found in only 7.69%, a single depressive episode was in 13.2%. Different degrees of cognitive impairment (CI) were observed in 91 (78.4%) patients. Multivariate analysis and linear regression were used to build a predictive model, from which it follows that ADSDs in patients with BD are primarily associated with sleep disorders (β=0.412), asthenia (β=0.149), CI (β=0.137), chronic stress (β=-0.010) and its severity (β=0.134), early childhood psychic trauma (ECPT) before the age 7 years (β=0.152), the development of ADSD before the onset of BD (β =0.160), older age of eye involvement in the pathological process (β=0.089), gastrointestinal tract (GIT) involvement within BD (β=0.096), high C-reactive protein (CRP) levels (β=0.177), and poor subjective status of patients (β=0.120) (area under the ROC-curve, 0.940). Conclusion. Chronic ADSDs are encountered with high frequency in patients with BD and frequently occur simultaneously with the latter or during its development. Their occurrence is favored to the greatest extent by ECPT and obvious chronic psychosocial stress preceding ADSDs. GIT involvement, late-onset ocular pathology, high CRP levels, and poor subjective status are common to patients with BD and ADSDs. Sleep disorders, asthenic syndrome, and CI are significant in the pattern of ADSDs.

© Springer Science+Business Media New York 2016. A comparative study performed in mice investigating the action of DF302, a novel fluoride-containing gamma-carboline derivative, in comparison to the structurally similar neuroprotective drug dimebon. Drug effects on learning and memory, emotionality, hippocampal neurogenesis and mitochondrial functions, as well as AMPA-mediated currents and the 5-HT6 receptor are reported. In the step-down avoidance and fear-conditioning paradigms, bolus administration of drugs at doses of 10 or 40 mg/kg showed that only the higher dose of DF302 improved long-term memory while dimebon was ineffective at either dosage. Short-term memory and fear extinction remained unaltered across treatment groups. During the 5-day predation stress paradigm, oral drug treatment over a period of 2 weeks at the higher dosage regimen decreased anxiety-like behaviour. Both compounds supressed inter-male aggression in CD1 mice, the most eminent being the effects of DF302 in its highest dose. DF302 at the higher dose decreased floating behaviour in a 2-day swim test and after 21-day ultrasound stress. The density of Ki67-positive cells, a marker of adult neurogenesis, was reduced in the dentate gyrus of stressed dimebon-treated and non-treated mice, but not in DF302-treated mice. Non-stressed mice that received DF302 had a higher density of Ki67-positive cells than controls unlike dimebon-treated mice. Similar to dimebon, DF302 effectively potentiated AMPA receptor-mediated currents, bound to the 5-HT6 receptor, inhibited mitochondrial permeability transition and displayed cytoprotective properties in cellular models of neurodegeneration. Thus, DF302 exerts multi-target effects on the key mechanisms of neurodegenerative pathologies and can be considered as an optimized novel analogue of the neuroprotective agent dimebon.

© 2018 Bentham Science Publishers. A number of biological and clinical characteristics typical of late life depression (LLD) have been suggested by recent research findings. The close association of LLD with cognitive impairment is now well documented and evidenced. However, it is still not clear whether it is depression that leads to cognitive decline, and in more severe cases, to dementia. The work presented in this review article suggests that depression and dementia frequently and strongly copresent, even if the causality remains largely opaque.

Цель исследования. Изучение связи между генами иммунной системы и депрессией, а также ее эндофенотипами (невротизм и личностная тревожность) при ишемической болезни сердца (ИБС). Материал и методы. Исследование проведено в группе мужчин с ИБС с депрессией (78 человек) и без нее (91 человек), а также у здоровых добровольцев мужского пола (127 человек). Изучены полиморфизмы генов интерлейкина-4 (IL-4 –589C/T), интерлейкина-6 (IL-6 –174G/C), фактора некроза опухолей-α (TNF-α –308G/A) и С-реактивного белка (CRP –717A/G). Результаты. Обнаружена ассоциация полиморфизма IL-6 –174 G/C с депрессией, коморбидной ИБС (р=0,01; ОШ=2,3 ДИ 95% 1,2—4,3), которая выражалась в повышении частоты высокоэкспрессивного аллеля G в группе больных с депрессией. Полиморфизм IL-4 –589C/T был ассоциирован с ИБС: частота генотипа СС IL-4 –589C/T была выше в группе больных по сравнению с контрольной группой независимо от наличия депрессии (р=0,007; ОШ=2,1 ДИ 95% 1,2—3,4). Полиморфизмы TNF-α –308G/A и CRP –717A/G не были ассоциированы с депрессией при ИБС. Значимых различий в выраженности невротизма и личностной тревожности у носителей различных генотипов по локусам IL-4 –589 C/T, IL-6 –174 G/C, TNF-α –308 G/A, CRP –717A/G выявлено не было. Заключение. Ассоциация полиморфизма IL-6 –174G/C с депрессией, коморбидной ИБС, согласуется с данными литературы о роли IL-6 в развитии депрессии у кардиологических больных.

Background: The vascular endothelial growth factor (VEGF) is a neuroprotective cytokine that promotes neurogenesis and angiogenesis in the brain. In animal models, it has been shown that environmental enrichment and exercise, two non-pharmacological interventions that are beneficial decreasing the progression of Alzheimer disease (AD) and depressive-like behavior, enhance hippocampal VEGF expression and neurogenesis. Furthermore, the stimulation of VEGF expression promotes neurotransmission and synaptic plasticity processes such as neurogenesis. It is thought that these VEGF actions in the brain, may underly its beneficial therapeutic effects against psychiatric and other neurological conditions.

Conclusion: In this review, evidence linking VEGF deficit with the development of AD as well as the potential role of VEGF signaling as a therapeutic target for cotinine and other interventions in neurodegenerative conditions are discussed.

A comparative study performed in mice investigating the action of DF302, a novel fluoride-containing gamma-carboline derivative, in comparison to the structurally similar neuroprotective drug dimebon. Drug effects on learning and memory, emotionality, hippocampal neurogenesis and mitochondrial functions, as well as AMPA-mediated currents and the 5-HT6 receptor are reported. In the step-down avoidance and fear-conditioning paradigms, bolus administration of drugs at doses of 10 or 40 mg/kg showed that only the higher dose of DF302 improved long-term memory while dimebon was ineffective at either dosage. Short-term memory and fear extinction remained unaltered across treatment groups. During the 5-day predation stress paradigm, oral drug treatment over a period of 2 weeks at the higher dosage regimen decreased anxiety-like behaviour. Both compounds supressed inter-male aggression in CD1 mice, the most eminent being the effects of DF302 in its highest dose. DF302 at the higher dose decreased floating behaviour in a 2-day swim test and after 21-day ultrasound stress. The density of Ki67-positive cells, a marker of adult neurogenesis, was reduced in the dentate gyrus of stressed dimebon-treated and non-treated mice, but not in DF302-treated mice. Non-stressed mice that received DF302 had a higher density of Ki67-positive cells than controls unlike dimebon-treated mice. Similar to dimebon, DF302 effectively potentiated AMPA receptor-mediated currents, bound to the 5-HT6 receptor, inhibited mitochondrial permeability transition and displayed cytoprotective properties in cellular models of neurodegeneration. Thus, DF302 exerts multi-target effects on the key mechanisms of neurodegenerative pathologies and can be considered as an optimized novel analogue of the neuroprotective agent dimebon.

A comparative study performed in mice investigating the action of DF302, a novel fluoride-containing gamma-carboline derivative, in comparison to the structurally similar neuroprotective drug dimebon. Drug effects on learning and memory, emotionality, hippocampal neurogenesis and mitochondrial functions, as well as AMPA-mediated currents and the 5-HT6 receptor are reported. In the step-down avoidance and fear-conditioning paradigms, bolus administration of drugs at doses of 10 or 40 mg/kg showed that only the higher dose of DF302 improved long-term memory while dimebon was ineffective at either dosage. Short-term memory and fear extinction remained unaltered across treatment groups. During the 5-day predation stress paradigm, oral drug treatment over a period of 2 weeks at the higher dosage regimen decreased anxiety-like behaviour. Both compounds supressed inter-male aggression in CD1 mice, the most eminent being the effects of DF302 in its highest dose. DF302 at the higher dose decreased floating behaviour in a 2-day swim test and after 21-day ultrasound stress. The density of Ki67-positive cells, a marker of adult neurogenesis, was reduced in the dentate gyrus of stressed dimebon-treated and non-treated mice, but not in DF302-treated mice. Non-stressed mice that received DF302 had a higher density of Ki67-positive cells than controls unlike dimebon-treated mice. Similar to dimebon, DF302 effectively potentiated AMPA receptor-mediated currents, bound to the 5-HT6 receptor, inhibited mitochondrial permeability transition and displayed cytoprotective properties in cellular models of neurodegeneration. Thus, DF302 exerts multi-target effects on the key mechanisms of neurodegenerative pathologies and can be considered as an optimized novel analogue of the neuroprotective agent dimebon.

Цель исследования. Изучение связи между генами иммунной системы и депрессией, а также ее эндофенотипами (невротизм и личностная тревожность) при ишемической болезни сердца (ИБС). Материал и методы. Исследование проведено в группе мужчин с ИБС с депрессией (78 человек) и без нее (91 человек), а также у здоровых добровольцев мужского пола (127 человек). Изучены полиморфизмы генов интерлейкина-4 (IL-4 –589C/T), интерлейкина-6 (IL-6 –174G/C), фактора некроза опухолей-α (TNF-α –308G/A) и С-реактивного белка (CRP –717A/G). Результаты. Обнаружена ассоциация полиморфизма IL-6 –174 G/C с депрессией, коморбидной ИБС (р=0,01; ОШ=2,3 ДИ 95% 1,2—4,3), которая выражалась в повышении частоты высокоэкспрессивного аллеля G в группе больных с депрессией. Полиморфизм IL-4 –589C/T был ассоциирован с ИБС: частота генотипа СС IL-4 –589C/T была выше в группе больных по сравнению с контрольной группой независимо от наличия депрессии (р=0,007; ОШ=2,1 ДИ 95% 1,2—3,4). Полиморфизмы TNF-α –308G/A и CRP –717A/G не были ассоциированы с депрессией при ИБС. Значимых различий в выраженности невротизма и личностной тревожности у носителей различных генотипов по локусам IL-4 –589 C/T, IL-6 –174 G/C, TNF-α –308 G/A, CRP –717A/G выявлено не было. Заключение. Ассоциация полиморфизма IL-6 –174G/C с депрессией, коморбидной ИБС, согласуется с данными литературы о роли IL-6 в развитии депрессии у кардиологических больных.

Background: The vascular endothelial growth factor (VEGF) is a neuroprotective cytokine that promotes neurogenesis and angiogenesis in the brain. In animal models, it has been shown that environmental enrichment and exercise, two non-pharmacological interventions that are beneficial decreasing the progression of Alzheimer disease (AD) and depressive-like behavior, enhance hippocampal VEGF expression and neurogenesis. Furthermore, the stimulation of VEGF expression promotes neurotransmission and synaptic plasticity processes such as neurogenesis. It is thought that these VEGF actions in the brain, may underly its beneficial therapeutic effects against psychiatric and other neurological conditions.

Conclusion: In this review, evidence linking VEGF deficit with the development of AD as well as the potential role of VEGF signaling as a therapeutic target for cotinine and other interventions in neurodegenerative conditions are discussed.