Table 3.

iPSC modeled Alzheimer’s disease.

Reference	Disease and mutation	Tested cells (induced from iPSC)	Phenotype reported	Effective drug treatment
Yagi et al., 2011	fAD: PS1 A246E mutation, PS2 N141I mutation	Neurons	Elevated Aβ42/Aβ40.	Compound E (γ-secretase inhibitor) and compound W (Aβ42 inhibitor) reduced Aβ42 and Aβ40. High dose compound W reduced Aβ42/Aβ40 ratio.
Israel et al., 2012	fAD: duplication of APP sAD	Neurons	Aβ(1-40), phospho-tau, aGSK-3β increase, large RAB5-positive early endosomes.	β-secretase inhibitor reduces phospho-tau and aGSK-3β.
Koch et al., 2012	fAD: PS1 L166P mutation, PS1 D385N mutation	iPSC and embryonic derived NSCs	Elevated Aβ42/Aβ40. Decreased Aβ40, while Aβ42 did not differ from control. Partial loss of γ-secretase function.	γ-secretase inhibitor and non-steroidal anti-inflammatory drugs reduce Aβ.
Duan et al., 2014	sAD: ApoE3/E4	Basal forebrain cholinergic neurons	Elevated Aβ42/Aβ40. Elevated sensitivity to calcium influx and glutamate toxicity.	Low dose of γ-secretase inhibitor elevates Aβ secretion in sAD, while it typically reduces Aβ in fAD.
Kondo et al., 2013	fAD: APP-E693Δ mutation and APP-V717L mutationsAD	Neurons	Intracellular Aβ aggregation in APP-E693Δ line, while no significant extracellular plaque aggregation was observed. Endoplasmic reticulum and oxidative stress response in APP-E693Δ line.	Docosahexaenoic acid (DHA) reduces stress response in APP-E693Δ and one of two sporadic patients.
Muratore et al., 2014	fAD: APP-V717L mutation	Neurons	Elevated Aβ42 and Aβ38. Increased β-secretase cleavage of APP. Altered γ-secretase cleavage site Hyperphosphorylated tau.	Aβ-specific antibody reduce elevated tau.
Sproul et al., 2014	fAD: PS1 A246E mutation, PS1 M146L mutation	Neural progenitor cells, neurons	Elevated Aβ42/Aβ40, more apparent in NPCs than neurons. 14 genes (e.g., NLRP2, ASB9, NDP) are recognized to alter expression in PS1 mutated patients’ NPCs, 5 of them involved in late-onset AD as well.
Hossini et al., 2015	sAD	Neurons	Elevated GSK3β activity and phosphorylated tau. Generate an AD-related protein network. Ubiquitin-proteasome system function is down-regulated in sAD.	γ-secretase inhibitor down regulates phosphorylated tau.
Moore et al., 2015	fAD: PS1 Y115C mutation, PS1 intron 4 mutation, APP V717I mutation, APP duplication	Neurons	All lines demonstrated increased Aβ42 generation. APP mutations show elevated phenotype while PS1 mutations did not.	γ-secretase inhibitor increased intracellular tau, β-secretase inhibitor reduced intracellular tau. γ-secretase modulation reduced intracellular tau.
Young et al., 2015	sAD: SORL1 SNPs (risk variants and Protective variants)	Neurons		BDNF treatment reduces Aβ by SORL1–dependent upregulation in protective homozygotes or heterozygotes. In risk homozygotes, BDNF treatment is not effective in reducing Aβ. Overexpression of SORL1 cDNA ameliorates Aβ.
Woodruff et al., 2016	fAD: PS1 ΔE9 mutation, APP V717F mutation, APP Swedish mutation	Neurons	APP and LDL endocytosis and soma-to-axon transcytosis of lipoproteins dysfunction in fAD.	β-secretase inhibitor recovers endocytosis function.
Jones et al., 2017	fAD and sAD	Astrocytes Neural progenitor cells	Atrophy and abnormal localization of astrocytes from both fAD and sAD, while NPCs did not show evident pathology.