Modeling Alzheimer’s Disease with Induced Pluripotent Stem Cells: Current Challenges and Future Concerns

Table 2

Human somatic cell reprogramming-based neuronal models of Alzheimer’s disease.

Disease	Genetic defect	Outcome	Drug test	Reference
Azheimer’s disease	PSEN1 A264E; PSEN2 N141I	Increase secretion of Aβ1–42 in neurons with mutations	γ-secretase inhibitors	Yagi et al., 2011 [80]
	Duplication of APP; Sporadic	Increase secretion of Aβ1–42 and phosphorylated tau (Thr231) in neurons with mutations	β-secretase inhibitors	Israel et al., 2012 [84]
	APP E693Δ; APPV717L; Sporadic	Increase of intracellular Aβ olimgo in neurons with APPE693Δ;	DHA	Kondo et al., 2013 [86]
	Asymptomatic and symptomatic APP V717I	Increase secretion of Aβ1–42 and Aβ1–38 in neurons with mutations	Aβ antibody	Muratore et al., 2014 [85]
	PSEN1 A246E; PSEN1 M146L	Gene expression differences between neurons with mutations of PSEN1 and controls	no	Sproul et al., 2014 [83]
	Sporadic	Changes in gene expression as well as the inducible subunits of the proteasome complex associated with AD in AD-iPS derived neuronal cells	γ-secretase inhibitors	Hossini et al., 2015 [87]