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[Preprint]. 2024 May 20:rs.3.rs-4313679. [Version 1] doi: 10.21203/rs.3.rs-4313679/v1

Figure 6. Rolipram suppresses Aβ42 oligomers neurotoxic effects on hiPSC-derived cortical neurons.

Figure 6

(A-D) Patch clamp electrophysiology recordings from the hiPSC-derived cortical neurons showed the blocking of the Aβ42-induced defects by co-treatment with rolipram (1 μM) for 24 hours, as demonstrated for the readouts of Sodium currents (A), AP amplitude (B), spontaneous firing rate (C) and amplitude (D). (E) Analysis of cell function on cortical-MEA systems showed a stimulus-induced increase in cell activity was maintained in control samples dosed with Aβscr (5 μM), but was completely abolished within 1h of Aβ42 oligomers dosing. This Aβ42-induced abolishment was blocked by co-treatment with rolipram (1 μM). Statistical analysis was computed using student t-test or One-Way ANOVA with Tukey’s test and Alpha (0.05) is significance. (N ≥ 18), *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, **** p ≤ 0.0001.