Fig. 2 | Scientific Reports

Fig. 2

From: Validation of a functional human AD model with four AD therapeutics utilizing patterned ipsc-derived cortical neurons integrated with microelectrode arrays

Fig. 2

Aβ42 oligomer-induced neurotoxicity of hiPSC-derived cortical neurons is inhibited by Donepezil for both patch clamp and MEA electrophysiological recordings. (A–D) Patch clamp electrophysiology recordings from the hiPSC-derived cortical neurons indicated the blocking of Aβ42-induced deficits by co-treatment with Donepezil (1 µM) for 24 h, as demonstrated for the readouts of sodium currents (A), action potential (AP) amplitude (B), spontaneous firing rate (C) and amplitude (D). (E) Analysis of cell function on patterned cortical MEA systems revealed a stimulus-induced increase in cell activity (i.e., firing frequency) was maintained in control samples dosed with Aβscr (5 µM), but was completely abolished within 1 h of Aβ42 oligomers dosing. However, this Aβ42-induced abolishment was blocked by co-treatment with donepezil (DNP, 1 µM). Statistical analysis was performed via one-way ANOVA followed by Fisher’s LSD (α = 0.05) (N ≥ 16), *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001.

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