Neuroscience
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Glucocorticoids (GCs) are widely used as powerful anti-inflammatory and immunosuppressive therapeutics in multiple pathological conditions. However, compelling evidence indicates that they might promote neurodegeneration by altering mitochondrial homeostatic processes. ⋯ In this report, we have compared the neurotoxicity induced by dexamethasone, prednisolone, betamethasone, and hydrocortisone in cultured neuroblastoma cells, through the analysis of several parameters such as cell viability, ER stress, oxidative stress, and mitochondrial fusion and fission markers. Interestingly, we have found that synthetic glucocorticoids may impact neuronal viability by affecting different cellular responses, suggesting that their therapeutic use should be consciously decided after careful consideration of benefits and detrimental effects.
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Auditory beats stimulation (ABS) has received increased attention for its potential to modulate neural oscillations through a phenomenon described as brain entrainment (i.e synchronization of brain's electrocortical activity to external stimuli at a specific frequency). Recently, a new form of ABS has emerged, inspired by isochronic tones stimulation (ITd). This study investigated neural oscillatory responses induced by ITd in comparison with formerly well-established ABS protocols, such as gamma-binaural beats (BB) and white noise (WN). ⋯ Findings also revealed that ITd elicited acute changes in the alpha band of EEG oscillations, through a progressive decrease in power over time, which was distinctly different from the pattern observed while listening BB and WN. Such dual alpha-gamma effects underline the promising and unique potential of ITd to modulate neural oscillations which selectively differ from BB and WN. This study contributes to the evolution of ABS research, highlighting the promise of ITd for cognitive enhancement and clinical applications.
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The study aimed to assess the analgesic effect of 10 Hz repetitive transcranial magnetic stimulation (rTMS) targeted to the prefrontal cortex (PFC) region on neuropathic pain (NPP) in rats with chronic constriction injury (CCI) of the sciatic nerve, and to investigate the possible underlying mechanism. Rats were randomly divided into three groups: sham operation, CCI, and rTMS. In the latter group, rTMS was applied to the left PFC. ⋯ The results showed that CCI caused NPP in rats, reduced the pain threshold, promoted microglial polarisation to the M1 phenotype, and increased the secretion of pro-inflammatory and anti-inflammatory factors. Moreover, 10 Hz rTMS to the PFC was shown to improve NPP induced by CCI, induce microglial polarisation to M2, reduce the secretion of pro-inflammatory factors, and further increase the secretion of anti-inflammatory factors. Our data suggest that 10 Hz rTMS can alleviate CCI-induced neuropathic pain, while the underlying mechanism may potentially be related to the regulation of microglial M1-to-M2-type polarisation to regulate neuroinflammation.
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Cerebral ischemia/reperfusion injury (CIRI) is a common feature of ischemic stroke leading to a poor prognosis. Effective treatments targeting I/R injury are still insufficient. The study aimed to investigate the mechanisms, by which glycyrrhizic acid (18β-GA) in ameliorates CIRI. ⋯ However, the JAK2/STAT3 activator colivelin TFA abolished the inhibitory effect of 18β-GA, suppressed autophagy, and significantly decreased the Bcl-2/Bax ratio. Taken together, these findings suggested that 18β-GA pretreatment ameliorated CIRI partly by triggering a protective autophagy via the JAK2/STAT3 pathway. Therefore might be a potential drug candidate for treating ischemic stroke.
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The progression of Alzheimer's disease (AD) has a silent phase that predates characteristic cognitive decline and eventually leads to active cognitive deficits. Metabolism, diet, and obesity have been correlated to the development of AD but is poorly understood. The hypothalamus is a brain region that exerts homeostatic control on food intake and metabolism and has been noted to be impacted during the active phase of Alzheimer's disease. ⋯ The results show a large panel of inflammatory mediators, leptin, and other proteins that may be involved in weakening the blood brain barrier, to be increased in the young AppNL-G-F mice but not in the old AppNL-G-F mice. There were also several differentially expressed genes in both the hypothalamus and the hippocampus in the young AppNL-G-F mice prior to amyloid plaque formation and cognitive decline that persisted in the old AppNL-G-F mice, including GABRa2 receptor, Wdfy1, and several pseudogenes with unknown function. These results suggests that a larger panel of inflammatory mediators may be used as blood markers to detect silent AD, and that a change in leptin and gene expression in the hypothalamus exist prior to cognitive effects, suggesting a coupling of metabolism with amyloid plaque induced cognitive decline.