The Potential of Induced Pluripotent Stem Cells to Treat and Model Alzheimer’s Disease

Table 1

Current genetic iPSC models of Alzheimer’s disease.

Gene	Model/mutation	Phenotype	References
APP	iPSC/KM670/671NL	Increased levels of Aβ p-tau (Thr231); GSK3B activity ↑; Neurodegeneration	[120, 121]
	iPSC/A673T	Decreases levels of sAPPβ; Neurodegeneration	[123]
	MSC/trisomy 21	Aβ expression ↑; p-Tau expression ↑; Neurodegeneration	[127]
PSEN1	iPSC/PSEN1δ9	Mutant astrocytes; Disrupted Ca2+ signaling in healthy neurons; Toxic Aβ secretion; Neurodegeneration	[128, 129]
MAPT	iPSC/IVS10+16, P301S	4R:3R tau expression increased; Perturbations in Ca^2+ burst frequency; Reduced lysosomal acidity; Tau oligomerization; Neurodegeneration	[132]
APOE	iPSC/APOER (, 3, or 4)	Allelic expression of APOE influences APP transcription through an; abnormal kinase cascade; APOE4 astrocytes and microglia exhibited a decrease in Aβ clearance; Accumulation of cholesterol in the intra- and extracellular matrices; Aβ expression led to the activation of microglia; however, the length of; processes was allelic dependent	[134, 137, 139]