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. 2016 May 24;2016:7828049. doi: 10.1155/2016/7828049

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]