Incidence of Parkinson disease progressively grows with increasing age and percentage of elderly people in the global population. Clear understanding of the causes of dopaminergic neurons death in Substantia nigra and Parkinson disease pathogenesis are currently absent, not speaking of an efficient therapy. However, an early diagnosis of dopaminergic neurons degeneration and prescription of dopamine replacement therapy significantly slow down the rate of symptoms progression. An increased concentration of iron in Substantia nigra of Parkinson disease patients has been shown in several studies. In this review we summarized the data concerning a potential significance of lactoferrin, the iron-binding protein of exocrine secretions and neutrophils, for early diagnosis and treatment of Parkinson disease. Salivary and lacrimal lactoferrin levels in Parkinson disease patients were higher than those observed in the control group. Plasma levels of lactoferrin inversely correlated with Parkinson disease severity even after treatment with Levodopa, a dopamine agonist, and with monoaminooxidase inhibitors. Lactoferrin levels in cerebrospinal fluid of Parkinson disease patients negatively correlated with the tumor necrosis factor-alpha concentration. Lactoferrin treatment of rodents with several experimental models of Parkinson disease (induced by rotenone, MPTP) protected neurons and mitigated the symptoms of neurodegeneration. Some contradictions about the positive effects of lactoferrin as a remedy in Parkinson disease animal models and possible participation of lactoferrin in accumulation of iron in neurons are discussed.

Introduction. Mutations in a GBA1 gene, which encodes a lysosomal enzyme called glucocerebrosidase (GCase), are the most common genetic risk factor for Parkinson's disease (PD). The pathogenesis of PD results from the death of dopaminergic neurons in the substantia nigra of the brain, which is associated with the aggregation of α-synuclein protein. However, not all GBA1 mutation carriers develop PD during their lifetime. The aim of this study was to evaluate GCase activity and α-synuclein levels in CD45+ blood cells of patients with PD associated with GBA1 mutations (GBА1-PD), asymptomatic carriers of GBA1 mutations (GBА1-carriers), and patients with sporadic PD (sPD), as well as correlation between the study parameters in the study groups. Materials and methods. The study included patients with GBА1-PD (n = 25) and sPD (n = 147), and GBА1-carriers (n = 16). A control group included healthy volunteers (n = 154). The level of α-synuclein in CD45+ cells was measured by enzyme-linked immunosorbent assay, and GCase activity in dried blood spots was detected by high-performance liquid chromatography with tandem mass spectrometry. Results. Increased level of α-synuclein protein was detected in CD45+ blood cells of patients with GBA1-PD, sPD, and GBA1-carriers compared to controls (p = 0.0043; p = 0.0002; p = 0.032, respectively). Decreased GCase activity was reported in GBA1-PD patients and GBA1-carriers compared to sPD patients (p = 0.0003; p = 0.003, respectively) and controls (p 0.0001; p 0.0001, respectively). However, negative correlation between α-synuclein levels and GCase activity was observed only in GBA1-PD patients, but not in GBA1-carriers. Conclusion. Our data suggest a possible functional relationship between the activity of GCase and the metabolism of α-synuclein in PD associated with GBA1 mutations.

Effective therapy of insomnia, especially chronic insomnia, is one of the most pressing neuropsychiatric problems. Unfortunately, at present in the Russian Federation, as in most other countries of the world, there are no officially approved drugs for long-term treatment of insomnia. In this regard, the use of medical sedation agents that do not have restrictions on the duration of use is of considerable interest. This review considers drugs of various psychopharmacological classes, one way or another used in practice for the correction of sleep disorders, especially in patients with underlying comorbid pathology.

Introduction. Modern neuroimaging methods allow to evaluate in vivo biochemical processes in the brain. Such methods include magnetic resonance spectroscopy (MRS) and positron emission tomography (PET). While PET is the “golden standard” in assessing the brain functional state and is widely used in neurodegenerative diseases, the diagnostic value of MRS remains undefined due to the inconsistency of the results obtained in different studies. At the same time, MRC allows obtaining information on the content of many metabolites in living tissues, including N-acetyl aspartate (NAA), which is considered to be a surrogate marker of neuronal integrity, choline (Cho), associated with membrane metabolism, Cr - energy metabolism, etc. The aim of this study is to compare MRS and PET data in patients with Parkinson’s disease (PD).Materials and methods. Twenty-six patients with PD stages I to III according to the Hoehn and Yahr Scale and age-matching control group of neurologically and cognitively intact people were examined. All patients underwent neurological examination, a multivoxel MRS of the supraventricular region, including white and gray matter, and PET with 18F-fluorodeoxyglucose (FDG) to assess cerebral metabolic rate of glucose (CMRglu).Results. Decrease of NAA/Cr and NAA/Cho in the white matter in the left hemisphere was revealed in PD group compared to control, with the NAA/Cr ratio negatively correlating with the stage of the disease of the Hoehn and Yahr Scale. The NAA content in the white matter and the cingulate cortex positively correlated with CMRglu in Brodmann fields 5–7, 8–10, 22, 23, 46. At the same time, Cho/Cr ratio negatively correlated with CMRglu in the cortical areas associated with the development of cognitive impairment in PD (Brodman areas 9, 10, 39, 47).

The posture is the position of the body in space, the ultimate goal of which is to maintain balance in static and dynamic conditions. The balance of the body is due to a complex system of regulation. The field of knowledge that studies balance maintenance processes is posturology. For over 20 years, stabilometry as a method of diagnosing postural balance has been widely used in clinical practice. This method has found its application in patients with pathologies of central and peripheral nervous systems. In this review we present modern concepts of postural balance formation and mechanisms of postural balance maintenance, as well as diagnostic capabilities of stabilometry in patients with diseases of extrapyramidal system.

The objective of the study was to validate our previous results obtained during the transcriptome analysis of the primary culture of peripheral blood macrophages in patients with Parkinson's disease associated with mutations in the GBA gene (GBA-PD) in that reduced expression of the neurogenesis genes EGR1 (early growth response protein 1), NR4A2 (nuclear receptor 4A2), JUNB (transcription factor jun-B) in patients with GBA-PD.Methods and materials. The study included 14 patients with GBA-PD, 15 GBA-carriers, 30 patients with Parkinson's disease (PD) and 44 persons of the control group. The assessment of relative mRNA level of neurogenesis genes EGR1, NR4A2, JUNB in peripheral blood mononuclear cells were carried out by real-time quantitative polymerase chain reaction (PCR) using TaqMan fluorescent probes or EvaGreen fluorescent DNA dye.Results. Relative mRNA level of the JUNB gene in peripheral blood mononuclears was decreased in the group of patients with GBA-PD compared to controls (p=0.034). We found out that the relative mRNA level of the NR4A2 gene in peripheral blood mononuclears was increased in the group of patients with GBA-carriers compared to GBA-PD, patients with PD and controls (p=0.0029, p=0.00045, p=0.0024 respectively). There were no statistically significant differences in the mRNA level of the EGR1 gene between all the study groups (p>0.05).Conclusion. GBA-PD is characterized by reduced expression of the JUNB gene compared to control and of the NR4A2 gene compared to GBA-carriers.