Effects of BT-11 treatment on hippocampal gene expression in Male Fisher transgenic 344-AD rats. [Male RNAseq]

5 month old Male Fisher transgenic 344-AD (Tg-AD) rats expressing human Swedish amyloid precursor protein (APPsw) and ? exon 9 presenelin-1 (PS1?E9) were treated with BT-11 (cat. no. HY-102013, MCE) at 8.5 mg/kg body weight administered in rodent chow. Following 6 months of BT-11 treatment, rats (11 months of age) were tested for cognitive behaviour prior to sacrificing. Hippocampal Brain region were dissected and RNA sequencing (RNAseq) analyses was done on the Isolated sample. Taken together we showed that BT-11 treatment enriched pathways in males including salt transmembrane transporter activity, signaling receptor regulator receptor ligand activity, signaling receptor activator activity, and transmembrane transporter activity. Overall design: To show the effects of BT-11-treatment on gene expression levels, Hippocampi of 5 BT-11 -treated and 5 untreated transgenic rats of male rats were analysed for gene expression by RNAseq. At 11 months of age, the rats were anaesthetized intraperitoneally with ketamine (100 mg/kg) and xylazine (10 mg/kg) and transcardially perfused with cold RNAse-free 1× PBS. Left hippocampi were removed and snap frozen for RNAseq analysis. Left hemisphere of the hippocampus. M1 – M5 (untreated male transgenic rats), MBT1 – MBT5 (transgenic male AD rats treated with the drug BT-11). Male Rats started BT-11 treatment at 5-months of age and were treated for 6 months untli they were 11 months old. For this experiment, the gene expression for the drug treated transgenic rats will be compared to that of the untreated transgenic group (MBT/M)