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REFERENCES 1. Mizuno K, Carnahan J, Nawa H. Brain-derived neurotrophic factor promotes differentiation of striatal GABAergic neurons. Dev Biol. 1994; 165(1): 243–256. 2. Bathina S, Das UN. Brain-derived neurotrophic factor and its clinical implications. Arch Med Sci. 2015; 11(6): 1164-78. 3. Zigova T, Pencea V, Wiegand SJ, Luskin MB. Intraventricular administration of BDNF increases the number of newly generated neurons in the adult olfactory bulb. Mol Cell Neurosci. 1998; 11: 234–45. 4. Carrasco MA, Castro P, Sepulveda FJ, Tapia JC, Gatica K, Davis MI, Aguayo LG

References 1. Numakawa T, Suzuki S, Kumamaru E, Adachi N, Richards M, Kunugi H. BDNF function and intracellular signaling in neurons. Histol Histopathol 2010; 25: 237-58. 2. Balaratnasingam S, Janca A. Brain derived neurotrophic factor: a novel neurotrophin involved in psychiatric and neurological disorders. Pharmacol Ther 2012; 134: 116-24. 3. Thoenen H. The changing scene of neurotrophic factors.Trends Neurosci 1991; 14: 165-70. 4. Aid T, Kazantseva A, Piirsoo M, Palm K, Timmusk T. Mouse and rat BDNF gene structure and expression revisited. J Neurosci Res 2007

Introduction Obesity is becoming a major health problem of modern society and affects all socio-economic categories, regardless of age, gender and ethnicity. Adolescent obesity is associated with metabolic, cardiovascular, psychological, orthopedic, neurological, respiratory and other disorders [ 1 , 2 ]. Of these, the most common is metabolic syndrome and type 2 diabetes mellitus (T2DM) [ 3 ]. Regarding the research of children and adolescent obesity and metabolic diseases, brain-derived neurotrophic factor (BDNF) is gaining increased interest. Brain-derived

;14:26. doi: 10.1186/1471-2202-14-26 9. Ghoneim FM, Khalaf HA, Elsamanoudy AZ, Abo El-khair SM, Helaly AMN, Mahmoud EM, Elshafey SH. Protective effect of chronic caffeine intake on gene expression of brain derived neurotrophic factor signaling and the immunoreactivity of glial fibrillary acidic protein and Ki-67 in Alzheimer’s disease. Int J Clin Exp Pathol 2015;8:7710-28. PMCID: PMC4555665 10. Mahdy KA, Gouda NAM, Marrie AH, Yassin NAZ, El- Shenawy SMA, Farrag ARH, Ibrahim BMM. Protective effect of ginger (Zingiber officinale) on Alzheimer’s disease induced in rats. J

(IGF-1) ( Mattson et al., 2007 ). IGF-1 and 5-HT play an important role in the expression of neurotrophic factors such as the brain-derived neurotrophic factor (BDNF) ( Carro et al., 2000 ; Mattson et al., 2004 ). This was evident after the artificial injection of IGF-1 into the peripheral blood vessel, which increased the expression of BDNF in the hippocampus of the brain after exercise ( Carro et al., 2000 ), and 5-HT was crucially involved, along with noradrenaline, in the regulatory mechanism that governed BDNF expression in the brain ( Mattson et al., 2004

morphological expression of neuropeptide Y (NPY) in cortical cultures by brain-derived neurotrophic factor (BDNF). Evidence for a requirement for extracellular-regulated kinase (ERK)-dependent and ERK-independent mechanisms. Brain Res., 919: 57–69. Benes V., Castoldi M. (2010). Expression profiling of microRNA using real-time quantitative PCR, how to use it and what is available. Methods, 50: 244–249. Byerly M.S., Simon J., Lebihan-Duval E., Duclos M.J., Cogburn L.A., Porter T.E. (2009). Effects of BDNF, T3, and corticosterone on expression of the hypothalamic obesity gene

adipose tissue thickness. Clin Exp Hypertens. 2015;37(6):505-10. DOI: 10.3109/10641963.2015.1013122 32. Rathcke CN, Vestergaard H. YKL-40, a new inflammatory marker with relation to insulin resistance and with a role in endothelial dysfunction and atherosclerosis. Inflamm Res. 2006;55(6):221-7. DOI: 10.1007/s00011-006-0076-y 33. Vermehren-Schmaedick A, Jenkins VK, Hsieh HY, Brown AL, Page MP, Brooks VL, et al. Upregulation of brain-derived neurotrophic factor expression in no-dose ganglia and the lower brainstem of hypertensive rats. J Neurosci Res 2013;91(2):220–9. DOI

Depression is a neuroprogressive disorder that is characterized by decreased neurogenesis and neurotrophic factors, including brain-derived neurotrophic factor (BDNF). Depression is associated with derangement of neurotransmitters such as serotonin, dopamine, noradrenaline, melatonin, and glutamate in the central nervous system (CNS) [ 1 , 2 ]. BDNF and lipid factors are potential biomarkers for depression. BDNF acts as a regulator of neuron growth. Various functions, such as regulating neuronal development, survival, durability, and plasticity of neurons, have

): Neurotrophins and their receptors in early development of the mammalian nervous system. Acta Neurobiologiae Experimentalis 70: 454–467. Benraiss A., Chmielnicki E., Lerner K., Roh D., Goldman S. A. (2001): Adenoviral brain-derived neurotrophic factor induces both neostriatal and olfactory neuronal recruitment from endogenous progenitor cells in the adult forebrain. Journal of Neuroscience 21: 6718–6731. Bowers D., McKenzie D., Dutta D., Wheeless C. R., Cohen W. R. (2001): Growth hormone treatment after caesarean delivery in rats increases the strength of the uterine scar


New achievements within structural and functional imaging of central nervous system offer a basis for better understanding of the mechanisms underlying many mental disorders. In everyday clinical practice, we encounter many difficulties in the therapy of eating disorders. They are caused by a complex psychopathological picture, varied grounds of the problems experienced by patients, often poor motivation for active participation in the treatment process, difficulties in communication between patients and therapeutic staff, and various biological conditions of eating disorders. In this paper, the latest reports on new concepts and methods of diagnosis and treatment of anorexia nervosa have been analyzed. The selection of the analyzed publications was based on the criteria taking into account the time of publication, the size of research cohorts, as well as the experience of research teams in the field of nutritional disorders, confirmed by the number of works and their citations. The work aims to spread current information on anorexia nervosa neurobiology that would allow for determining the brain regions involved in the regulation of food intake, and consequently that may be a potential place where neurobiochemical processes responsible for eating disorders occur. In addition, using modern methods of structural imaging, the authors want to show some of the morphometric variations, particularly within white matter, occurring in patients suffering from anorexia nervosa, as well as those evaluated with magnetoencephalography of processes associated with the neuronal processing of information related to food intake. For example as regards anorexia nervosa, it was possible to localize the areas associated with eating disorders and broaden our knowledge about the changes in these areas that cause and accompany the illness. The described in this paper research studies using diffusion MRI fiber tractography showed the presence of changes in the white matter pathways of the brain, especially in the corpus callosum, which indicate a reduced content of myelin. These changes probably reflect malnutrition, and directly represent the effect of lipid deficiency. This leads to a weakening of the structure, and even cell death. In addition, there are more and more reports that show the normal volume of brain cells in patients with long-term remission of anorexia. It was also shown that in patients in remission stage there are functional changes within the amygdala in response to a task not related symptomatologically with anorexia nervosa. The appearing in the scientific literature data stating that in patients with anorexia nervosa there is a reduced density of GFAP + cells of the hippocampus and increased expression of vimentin and nestin, is also worth noting.