In a recent work published in 2015, Nieweg et al. used human iPSC-derived cortical neurons, differentiated using an EB system similar to that applied by Li et al. (2015), to produce a highly reproducible cellular AD model that facilitates the mechanistic analysis of Aβ-induced synaptic pathomechanisms and the development of new therapeutic approaches (Nieweg et al., 2015). The differentiation protocol described by Li et al. states culturing iPSCs in a neural medium comprising Dulbecco's Modified Eagle Medium (DMEM)/F12, N2 supplement and heparin without growth factors (Li et al., 2009). Nieweg et al. (2015) used a modified medium that comprises of N2B27 medium (50% DMEM/F12, 50% Neurobasal), Glutamax, penicillin, streptomycin, modified N2 supplement, β-mercaptoethanol, 1% B27 without vitamin A and heparin. In the same paper, an attempt was made to recapitulate the synaptotoxicity of Aβ which is crucial for understanding the cascade of events leading to cell death and continuous brain degeneration. The cells were differentiated into deep layer cortical pyramidal neurons and GABAergic interneurons; and upon longer cultivation, these cells exhibited action potential generation and excitatory and inhibitory synapses. Yet,
