Болезнь Паркинсона (БП)-неуклонно прогрессирующее нейродегенеративное заболевание, проявляющееся как моторными, так и немоторными симптомами [1]. Биохимическим субстратом развития БП является прогрессирующая дегенерация дофаминергических нейронов черной субстанции, приводящая к дефициту дофамина [2]. Тем не менее в последнее время особое внимание уделяется изучению влияния и других нейромедиаторных систем на процессы патогенеза и формирование различных клинических проявлений БП [3]. На сегодняшний день появляется все больше данных, свидетельствующих о том, что глутамат (основной возбуждающий нейротрансмиттер ЦНС) играет важную роль в развитии БП [4]. В норме он активно участвует в процессах работы коры больших полушарий и гиппокампа за счет регуляции механизмов обучения и памяти [5], однако в избыточном количе

Hepcidin, a hormone regulating iron metabolism, has received attention for its role in the pathogenesis of dysregulations in carbohydrate metabolism. Hepcidin disorders in patients with diabetes mellitus are bi-directional: manifesting as iron overload syndrome in cases of decreased hepcidin production and as anaemia of chronic disease in cases of hepcidin hypersecretion. However, till date, detailed analyses of mechanisms underlying hepcidin dysregulation have not been conducted nor have the interactions of ferrocinetic and carbohydrate-metabolic disorders been examined. An association between diabetes mellitus and neurodegenerative diseases as well as the role of iron metabolism in Alzheimer or Parkinson diseases is a subject of ongoing research. This review provides a summary of the current understanding of hepcidin regulation and its disorders in various diseases, including diabetes mellitus and neurodegenerative diseases. In addition, we provide an overview of the available therapies that address ferrocinetic disorders resulting from the dysregulation of hepcidin.

This literature review is devoted to the study of recent advances in the field of neurorehabilitation using robotic technologies. Objective: to study best practices of applying robotic rehabilitation technologies in stroke patients, its clinical efficacy and influence on the molecular mechanisms of neuroplasticity. Keywords were searched in the Web of Science, Core Collection, Scopus and PubMed databases.Results.Robotic neurorehabilitation occupies a certain place in the comprehensive rehabilitation of patients with motor deficiency after stroke. An interdisciplinary patient-oriented approach and consistency at all stages of medical rehabilitation are especially important when using rehabilitation methods that implement advances in robotics and information technologies in patients after stroke. Rehabilitation with the use of high-tech computerized rehabilitation systems operating in the biofeedback mode is one of the promising areas and requires further neurophysiological and laboratory studies to create scientifically based methodological approaches. It will have great social significance and tangible economic effects from improving the quality of neurorehabilitation and reducing its duration.

Clinical variants of Parkinson's disease (PD) are not restricted to motor symptoms but include a wide spectrum of different non-motor symptoms: cognitive, psychotic, autonomic and sensory. These non-motor symptoms often occur long before classical motor features. Associated pathologic changes can now be identified at earliest stages using neuroimaging, pathomorphological and genetic studies. Therefore, PD is currently considered as a multifactorial, heterogenic systemic disease associated with involvement of multiple neurotransmitter systems. This leads to understanding that not only dopaminergic but also other neurotransmitter systems, including glutamatergic system, are involved in the pathogenesis of PD. This article aimed at investigating a role of glutamatergic system in the initiation of neurodegenerative process. The role of glutamate as a neurotransmitter and a neurotoxin in the pathogenesis of PD and progression of its clinical manifestations is discussed. The authors suggest that research into glutamate excitotoxicity in PD patients might allow the improvement of treatment tactics and correction of pathogenetic therapy.

The data we received in our study allow better understanding of PD pathogenesis.