Here, we found that a well-established animal model of hyperglycaemia, i.e., the STZ-injected mice, exhibited memory deficits (Figure 1B) associated with molecular changes in the hippocampus including lower amounts of NMDA receptor subunits GluN1 and GluN2a (Figure 1C), reduced phosphorylation levels of memory-related transcription factor CREB (Figure 1C) and decreased expression of genes encoding for synaptic proteins regulating synaptic transmission and plasticity such as SYT2, SYT4 and BDNF (Figure 1D). The gene discussed is BDNF; the disease is Hyperglycemia.