Topic: SH-SY5Y neuroblastoma cells

Type 2 diabetes mellitus (T2DM) is associated with a nearly 2-fold increased risk of Alzheimer's disease (AD) development although the reasons for this are unknown. Recent studies have reported dysregulated hippocampal neurogenesis in AD patients during postmortem examinations. Additionally, impaired neurogenesis has been observed in T2DM mouse models, suggesting this could explain the connection between T2DM and AD. This study aims to investigate how exposure to fatty acids associated with T2DM affects neuronal differentiation, serving as a model of neurogenesis. Human SH-SY5Y neuroblastoma c

The autism spectrum disorder (ASD)-associated 16p11.2 gene quinolinate phosphoribosyltransferase (QPRT) is essential for neuronal differentiation but not proliferation of SH-SY5Y neuroblastoma cells. QPRT is part of tryptophan metabolism and catabolizes quinolinic acid (QUIN), a NMDA-R agonist neurotoxic for glutamatergic cells. However, we can exclude a QUIN-driven neurotoxicity in the SH-SY5Y model. In primary human neural progenitor cells, chemical inhibition of QPRT using phthalic acid (PA) leads to premature differentiation and a shift from neurons to astrocytes. Here, we employed cerebra

Cytokine receptor-like factor 3 (CRLF3) is an phylogenetically ancient class 1 cytokine receptor present in all major eumetazoan taxa ranging from cnidarians to mammals. In humans, CRLF3 is expressed in various tissues and has been associated with proliferation, differentiation, cell survival and some diseases. Our studies on insect neurons and human iPSC-derived neurons demonstrated that CRLF3 (whose insect-endogenous ligand is still unidentified) can be activated by human erythropoietin (EPO) and its non-erythropoietic splice variant EV-3. Under apoptogenic conditions, CRLF3 initiates pro-su