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

5 month old Female Fisher transgenic 344-AD (Tg-AD) rats expressing human Swedish amyloid precursor protein (APPsw) and Δ exon 9 presenelin-1 (PS1ΔE9) 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 behavior 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 for females included passive transmembrane transporter activity, G protein-coupled receptor activity, G protein-coupled peptide receptor activity. 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. F1 – F5 (untreated female transgenic rats), FBT1 – FBT5 (transgenic female AD rats treated with the drug BT-11). Female 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 (FBT/F)