Fig. 7
From: Modifying Rap1-signalling by targeting Pde6δ is neuroprotective in models of Alzheimer’s disease
REM treatment reduces ERK1/2 signalling, Tau phosphorylation and cognitive impairments in mouse models of AD. a Western blot analysis quantifying p-ERK1/2 ratio to total ERK1/2 (n = 6 vehicle or 5 REM treated mice; P = 0.0220; t = 2.763; DF = 9) or b phosphorylated Tau at epitope: pS262 ratio to total tau (Vehicle: n = 4 mice; REM: n = 5 mice; P = 0.0007; t = 5.735; DF = 7) in cortex of transgenic hAPP*PS1 mice treated for 2 weeks with vehicle or REM0043039. Representative immunoblots are shown in inset above the graph. c REM significantly decreases pathological tau phosphorylation on epitope S262 compared to total tau also in the brainstem of tau P301L transgenic mice (n = 9 vehicle and 13 REM treated mice; P = 0.0217; t = 2.491; DF = 20). d Escape latency during MWM training comparing WT to hAPP mice with or without REM (n = 12 mice per condition; t-test: WT Vehicle/hAPP Vehicle: day 2 P = 0.0083; t = 2.901; DF = 22; day 3 P = 0.0153; t = 2.629; DF = 22; day 4 P = 0.00431; t = 3.183; DF = 22; hAPP Vehicle/REM: day 4 P = 0.056; t = 2.015; DF = 22; WT Vehicle/hAPP REM: day 1(b-d) P = 0.034; t = 2.256; DF = 22; day 2 P = 0.0264; t = 2.381; DF = 22 e Graphs showing the annulus crossing index (ACI) representing the number of crossings over the platform site in the target area adjusted for crossings over corresponding areas in other quadrants during the probe test (n = 12 mice per condition; ACI: Vehicle WT/ Vehicle hAPP: P = 0.0069; t = 2.98; DF = 22; hAPP Vehicle/REM: P = 0.0098; t = 2.829; DF = 22)). (One data-point from hAPP vehicle group is below 0 and is included in the analysis but not shown in the graph)