Table 1.

iPSC-derived in vitro studies to model AD and analyse disease-related mechanisms and phenotypes.

AD patient-derived iPSCs: genetic mutation	differentiation into cell type	differentiation marker	result	references
PSEN1 mutation A246E	basal forebrain cholinergic neurons	Tuj-1, amyloid-beta	an increased amyloid-beta 42 : 40 ratio	[36]
(APP)-E693D mutation	neurons and astrocytes with an accumulation of amyloid-beta oligomers	Tuj-1, GFAP, amyloid-beta	the accumulation of amyloid-beta oligomers in neurons and astrocytes	[37]
V717I mutation	neurons with reduction of total tau	Tuj-1, amyloid beta, tau	increases in APP expression and reduction of total tau	[38]
APP variant (A673T)	neurons with reduction of amyloid-beta	Tuj-1, amyloid beta,	neurons reduced levels of amyloid-beta	[39]
PS1 (A246E) and PS2 (N141I) mutations	neuron with elevated amyloid-beta 42 : 40	Tuj-1, amyloid beta	significant increase in expression of amyloid beta	[40]
PSEN1 mutation	neuron with increased amyloid-beta 42/40	Tuj-1, amyloid beta	significant increase in expression of amyloid beta	[41]