The treatment of various types of dementia remains a challenging task for psychiatry and neurobiology. This group of diseases is characterized by progressive impairment of cognitive functions and memory, accompanied by neurodegenerative processes in different areas of the brain. Drug treatment does not halt the degeneration of nervous tissue. Cell therapy using neural stem/progenitor cells is considered a promising approach for the treatment of various types of dementia. This paper discusses the unique properties and possible mechanisms of the influence of these cells after transplantation on the regeneration of nervous tissue, as well as specific examples of using the neural stem/progenitor cells from various sources in different types of dementia. Based on the analyzed data, it can be concluded that the olfactory mucosa might be a promising and accessible source for the creation of autologous cell-based preparation. Therefore, further research is needed on the use of olfactory mucosal neural stem/progenitor cells in the context of dementia.
Autism spectrum disorder (ASD) is a heterogeneous group of neurodevelopmental disorders characterized by deficits in social interaction, stereotypic behavior, and restricted interests. In ASD, dysregulation of proteins associated with synaptic plasticity, particularly brain-derived neurotrophic factor (BDNF), as well as elevated levels of inflammation, are observed. Investigating the involvement of BDNF in the pathogenesis of ASD and the search for new therapeutic agents represent an important task in psychopharmacology. The aim of this study was to investigate the effects of the low-molecular-weight dipeptide BDNF mimetic hexamethylenediamide bis(N-monosuccinyl-L-seryl-L-lysine) (GSB-106) on behavioral features and inflammation in rats with experimental ASD. ASD was modeled by administering valproic acid (VPA) at a dose of 600 mg/kg to female Wistar rats on gestational day 12.5. The offspring (both males and females) received GSB-106 orally at a dose of 0.1 mg/kg daily from postnatal day 7 (P7) to P81. From P39 to P81, stereotypic behavior, exploratory and locomotor activity, and pain sensitivity were assessed, followed by evaluation of inflammation by measuring complement system activity and the content of multiple-modified low-density lipoproteins (mmLDL). GSB-106 at a dose of 0.1 mg/kg reduced stereotypy 2.0-fold (p < 0.05), increased exploratory activity 1.3-fold (p < 0.05), and improved locomotor coordination 1.5-fold (p < 0.05) in male rats with ASD compared to the VPA group. In female rats with ASD, GSB-106 increased the pain threshold 1.2-fold (p < 0.05) and improved locomotor coordination 1.9-fold (p < 0.001). The effect of GSB-106 on metabolic and oxidative processes associated with inflammation was observed only in male rats with experimental ASD, as evidenced by a 39.9
Pregnancy in mammals is accompanied by deep restructuring of the cardiovascular system to provide adequate blood supply to the fetus and to maintain maternal homeostasis, where blood pressure and heart rate variability serve as important indicators of the system’s state and the effectiveness of its regulation mechanisms. The study investigated changes in hemodynamic parameters in pregnant and non-pregnant rats in response to acute hypoxic stress, experienced at different periods of gestation. It was shown that normal pregnancy is accompanied by a physiological decrease in blood pressure and a restructuring of autonomic regulation with activation of the sympathetic branch and a decrease in parasympathetic activity with a stable heart rate. Hypoxia in early pregnancy caused a significant and prolonged decrease in blood pressure, while in late gestation there were no blood pressure changes in response to the lack of oxygen but bradycardia persisted in both cases. Moreover, females exposed to hypoxia in late gestation demonstrated increased heart rate variability with activation of the parasympathetic system the following day. The dysregulation observed could cause long-term consequences, increasing the risk of cardiovascular diseases and impairing the adaptive potential of the mother’s body.
Due to the growing pollution of the environment with a microplastic (MP), the problem of MP impact on human health is relevant. MP is considered to contribute to the development of inflammatory bowel diseases. Therefore, we assessed the effect of long-term MP consumption on the expression of genes associated with the colon barrier function and on the luminal microflora composition in healthy mice and in mice with acute colitis. The effect of MP was modeled by replacing drinking water with a 10 mg/L suspension of 5 µm polystyrene particles for six weeks. To model acute colitis, 1
Metabolic syndrome (MS), a global problem of the 21st century, is characterized by hypertension, which is caused by the predominance of vasoconstriction over vasodilation. Hydrogen sulfide (H2S) is a recognized endogenous gas signaling molecule that has a variety of biological effects, including changes in vascular tone. The aim of this work was to study changes in contractile activity in isolated rat aorta in response to sodium hydrosulfide (NaHS), an H2S donor, and endogenous H2S during metabolic disturbances induced by a high-calorie (Western) diet. The study was performed on mature male Wistar rats. The diet resulted in the development of metabolic disturbances typical for MS. The results of a myographic study of thoracic aortic segments indicated that, in both the control and experimental groups, the administration of NaHS, depending on its concentration, resulted in bimodal effects, causing vasoconstriction at low concentrations and significantly more pronounced vasodilation at high concentrations. The effect of endogenous H2S depends on the state of perivascular adipose tissue and decreases in MS. Thus, the increase in H2S-induced vasodilation in MS is likely reflects a compensatory response to a decrease in endogenous H2S production. ATP-sensitive potassium channels play a leading role in mediating relaxation responses of aortic smooth muscle to H2S. However, their contribution to the development of vasodilation is less pronounced in MS, which is a consequence of changes in the involvement of other mechanisms. A decrease in H2S-induced vasoconstriction in MS, caused by increased superoxide anion production, may be one of these mechanisms. The interaction of various pathways for the implementation of H2S-induced vasorelaxation in metabolic disorders represents an important direction for further research to prevent the development of vascular diseases, including by regulating vascular tone.
