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

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 corresponds to cell-type specific RNA-sequencing of ECII neurons in vivo 1 week after DEK silencing using AAV vectors. Overall design: We injected ECII-bacTRAP mice stereotaxically with either control AAV or AAV expressing a small hairpin RNA directed against DEK. After 1 week, we lysed the entorhinal cortex (EC) from these mice, immunoprecipitated active polysomes, and then purified RNA for RNA-sequencing