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. 2024 Oct 22;14:24875. doi: 10.1038/s41598-024-73869-9

Fig. 6.

Fig. 6

Rolipram suppresses Aβ42 oligomer neurotoxic effects on hiPSC-derived cortical neurons. (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 h, 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 1 h of Aβ42 oligomer dosing. This Aβ42-induced abolishment was blocked by co-treatment with Rolipram (1 µM). Statistical analysis was performed via one-way ANOVA followed by Fisher’s LSD (α = 0.05). (N ≥ 18), *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001.