Neuroscience
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Pompe disease, also known as Glycogen storage disease type II, is an autosomal recessive disorder caused by defects in alpha-glucosidase, resulting in abnormal glycogen accumulation. ⋯ Quantitative data on the global epidemiology of Pompe disease could be the fundamental to evaluate the global efforts on building a better world for Pompe disease patients.
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The first of our aims in this study was to investigate the effects of 5-HT2AR, 5-HT7R, and A2AR blockades on miR-27b-3p expression in the short and long-term in neuroblastoma cells. Our second aim was to reduce the expression of pERK and suppress proliferation by blocking the 5-HT2AR with ketanserin. Our third aim was to reduce the expression of pAKT and induce apoptosis by blocking the A2AR and 5-HT7R with MSX3 and SB269970. ⋯ These findings showed that pAKT protein expression induced apoptosis due to decreased in neuroblastoma cells. Our study provides the first evidence for the relationships between ketanserin/miR-27b-3p/pERK, MSX3/miR-27b-3p/pAKT, and SB269970/miR-27b-3p/pAKT in neuroblastoma cells. Ketanserin, MSX3, and SB269970 drug combinations may be promising therapeutic agents in neuroblastoma cells.
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A growing number of studies show that the diabetes drug Semaglutide is neuroprotective in Alzheimer's disease (AD) animal models, but its mode of action is not fully understood. In order to explore the mechanism of Semaglutide, 7-month-old APP/PS1/tau transgenic (3xTg) mice and wild-type (WT) mice were randomly divided into four groups: control group (WT + PBS), AD model group (3xTg + PBS), Semaglutide control group (WT + Semaglutide) and Semaglutide treatment group (3xTg + Semaglutide). ⋯ Semaglutide can inhibit the apoptosis of BV2 cells induced by Aβ1-42 in a dose-dependent manner and promote the transformation of microglia from M1 to M2, thereby exerting anti-inflammatory and neuroprotective effects. Therefore, we speculate that Semaglutide shows an anti-inflammatory effect by promoting the transformation of microglia from M1 to M2 type in the brain of 3xTg mice, and thus exerts a neuroprotective effect.
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Alzheimer's disease (AD) and Parkinson's disease (PD) are neurodegenerative disorders that significantly impact well-being. Hyperoside (HYP), a flavonoid found in various plant species, particularly within the genus Hypericin, exhibits diverse pharmacological properties. However, the precise mechanisms underlying the anti-AD and anti-PD effects of HYP remain unclear. ⋯ We systematically assessed the neuroprotective potential of HYP in in vivo and in vitro models of AD and PD. Our findings indicated that HYP can mitigate, intervene in, and treat AD and PD animal models and associated cells through various mechanisms, including anti-oxidative, anti-inflammatory, anti-apoptotic, anti-Aβ aggregation, and cholinesterase inhibitory activities. Therefore, HYP potentially exerts anti-AD and anti-PD effects through diverse mechanisms, making it a promising candidate for therapeutic intervention in both AD and PD.
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The intercellular communication within the central nervous system (CNS) is of great importance for in maintaining brain function, homeostasis, and CNS regulation. When the equilibrium of CNS is disrupted or injured, microglia are immediately activated and respond to CNS injury. Microglia-derived exosomes are capable of participating in intercellular communication within the CNS by transporting various bioactive substances, including nucleic acids, proteins, lipids, amino acids, and metabolites. ⋯ Meanwhile, we summarized the molecular mechanisms by which the relevant exosomes exert regulatory effects. Exosomes, derived from microglia stimulated by different environments, regulate other nerve cells during the repair of CNS injury, having beneficial or detrimental effects on CNS repair. A comprehensive understanding of the molecular mechanisms underlying their role can provide a robust foundation for the clinical treatment of CNS injury.