Table 1.

iPSC models from patients with sporadic AD

sAD line	Cell type(s)	Phenotype(s)	Disease APOE genotype	Additional culture conditions	Environmental or genetic risk factor	Experimental results
Balez et al. [154]	Neurons	↑ Aβ42			H2O2, NO	↑ neurite retraction, apoptosis, hyper-excitable Ca2+ signalling
Birnbaum et al. [29]	Neurons (iN)	↑ ROS, ↑ DNA damage	E3/E3, E3/E4
Chen et al. [86]	Neurons			3D neuro-spheroid		Neuronal dysfunction similar to AD brain tissue
Duan et al. [123]	BFCNs	↑ Aβ42:40	E3/E4		Ionomycin, L-glutamate	↑ excitotoxicity
Hossini et al. [28]	Neurons	↑ GSK3β
Israel et al. [11]	Neurons	↑ Aβ40, ↑ p-tau, ↑ GSK3βa	E3/E3	+ Human astrocytes (Lonza)		↑ very large early endosomes
Jones et al. [55]	Astrocytes	Altered S100β, EAAT1, GS and inflammatory mediators expression and localisation	E4/E4
Kondo et al. [33]	Neurons, Astrocytes	↑ ER stress, ↑ OS, ↑ Aβ oligomersa		+ astrocytes of same iPSC line		↑ ROS ↑ Aβ oligomers
Lee et al. [85]	Neurons			3D neuro-spheroid
Lin et al. [56]	Neurons Astrocyte Microglia-like	↓ Aβ uptake, ↑ Aβ42	E4/E4, E3/E3	Organoids		↑ p-tau
Ochalek et al. [12]	Neurons	↑ Aβ42:40, ↑ APP, ↑ GSK3β, ↑ p-tau			Aβ oligomers, H2O2	↑ sensitivity to OS
Young et al. [30]	Neurons				SORL1
Balez et al. [154]	NSCs	↓SORL1	E4/E4

BFCNs basal forebrain cholinergic neurons, ER endoplasmic reticulum, NSC neural stem cells, OS oxidative stress, ROS reactive oxygen species

^aPhenotypes not observed in all sAD lines in study