The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [RNA-seq_invitro]

Neurons from layer II of the entorhinal cortex (ECII) are the first to accumulate tau protein aggregates and degenerate during prodromal Alzheimer’s disease. We used a data-driven functional genomics approach to model ECII neurons in silico that led us to the prediction that the proto-oncogene DEK is a driver of tau pathology in these neurons. In order to understand the function of DEK in vulnerable neurons, we modulated its expression in ECII neurons in vitro and in vivo in the mouse. The present GEO entry includes all of the data we collected from DEK-silenced and DEK-overexpressing ECneurons in vitro and in vivo. For the in vitro data, we generated primary neuron cultures of EC from mouse embryos at E17. At 7 days in vitro, we transduced the cultures with AAVs carrying shRNAs for DEK silencing (or the corresponding control non-targetting shRNA) or DEK cDNA for overexpression (or the corresponding empty control). 4 days post transduction, samples were harvested for RNAseq.