Targeting KCNN4 channels modulates microglial activation and apoptosis in a PD-relevant inflammatory model.

Parkinson's disease (PD) is characterized by chronic neuroinflammation and progressive dopaminergic neurodegeneration, driven primarily by the activation of microglia and associated apoptotic pathways. The intermediate-conductance calcium-activated potassium channel KCNN4 has recently emerged as a potential therapeutic target, yet its role in chronic neurodegenerative conditions remains underexplored. In this study, we investigated whether pharmacological inhibition of KCNN4 using TRAM-34 can modulate both inflammatory and apoptotic responses in an LPS-induced mouse model of PD.

Indoxyl sulfate is associated with cognitive impairment in ESRD patients by activating the extrinsic apoptosis in the neuronal cells during differentiating process.

This study investigates the correlation between indoxyl sulfate (IS) levels and cognitive impairment in end-stage renal disease (ESRD) patients from human study, and study. Comparison of demographic and biochemical data, including IS concentrations, was conducted between a control group(n=16) and the ESRD with cognitive impairment group (n=14) and without cognitive impairment (n=17). A CKD animal model induced renal impairment in adenine-fed C57BL/6 mice, assessing memory loss and behavioral changes.

GM1 ganglioside protects against LPS-induced neuroinflammatory and oxidative responses by inhibiting the activation of Akt, TAK1 and NADPH oxidase in MG6 microglial cells.

GM1 is a major brain ganglioside that exerts neurotrophic, neuroprotective and antineuroinflammatory effects. The aim of this study was to obtain insights into the antineuroinflammatory mechanisms of exogenous GM1 in lipopolysaccharide (LPS)-stimulated MG6 mouse transformed microglial cell line. First, we found that GM1 prevented the LPS-induced transformation of microglia into an amoeboid-like shape.

Lysosomal Dysfunction and Autophagy Blockade Contribute to MDMA-Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells.

Methylenedioxymethamphetamine (MDMA) is a psychostimulant with high abuse potential and severe neurotoxicity. According to our previous study, MDMA promotes autophagosome accumulation and contributes to cell death in cultured cortical and serotonergic neurons. However, the detailed mechanism underlying autophagy dysfunction remains unclear.

Autophagy inhibition plays a protective role against 3, 4-methylenedioxymethamphetamine (MDMA)-induced loss of serotonin transporters and depressive-like behaviors in rats.

The 3,4-methylenedioxymethamphetamine (MDMA) is a popular recreational drug, which ultimately leads to serotonergic (5-HT) neurotoxicity and psychiatric disorders. Previous in vitro studies have consistently demonstrated that MDMA provokes autophagic activation, as well as damage of 5-HT axons and nerve fibers. So far, whether autophagy, a well-conserved cellular process that is critical for cell fate, also participates in MDMA-induced neurotoxicity in vivo remains elusive.

Photoluminescent C-dots@RGO for sensitive detection of hydrogen peroxide and glucose.

We have demonstrated sensitive detections of hydrogen peroxide (H2O2) and glucose using reduced graphene oxide decorated with carbon dots (C-dots@RGO). The C-dots@RGO prepared from catechin (reducing agent and carbon source) and graphene oxide via hydrothermal routes possesses excitation-wavelength-dependence photoluminescence (PL) characteristics, with maximum excitation and emission wavelengths of 365 and 440 nm, respectively. The C-dots@RGO is stable in solution containing NaCl up to 350 mM, but is quenched by reactive oxygen species (ROS).

Synthesis of aluminum oxide supported fluorescent gold nanodots for the detection of silver ions.

Photoluminescent gold nanodots (Au NDs) on aluminum oxide nanoparticles (Al2O3 NPs) with the emission wavelengths ranging from 510 to 630 nm are unveiled. Orange Al2O3 NP@AuNDs show high selectivity and sensitivity towards Ag(+) ions by metallophilic Ag(+)-Au(+) interactions and induced fluorescence quenching of Au NDs.