Table 1.
iPSc models of Alzheimer’s disease.
| Genetic Defect | Affected Process(es) | Disease Type, iPS/hES N and n * | Transgene-Free? | Investigated Cell Type(s) | Reference(s) |
|---|---|---|---|---|---|
| APP | Aβ production and aggregation, MAPT | Familial early-onset (N = 2, father + daughter; n = 2 pre-selected) | N | Neurons | [31] |
| APP | Aβ production, ER stress | Familial early-onset (N = 2, n = 2 and 3) and sporadic (N = 2; n = 2) | Y | Cortical neurons, astrocytes | [32] |
| PSEN1 | β-amyloid processing | Early-onset AD, OE model in N = 1 hES and N = 1 iPS | Y/N | Neurons | [33] |
| PSEN1, PSEN2 | β-amyloid processing | Early-onset AD, N = 2 PSEN1&2; n = 2 | N | Neurons | [34] |
| ApoE(4) | Aβ levels | Early and late-onset DA, familial (N = 2) and sporadic (N = 3) | N | Basal forebrain cholinergic neuron | [35] |
| PSEN1 | Aβ production and aggregation, MAPT | Familial AD, N = 4 | N | Neural stem cells, neurons | [36] |
| APP and PSEN1 OE | Aβ production and processing | OE models of familial AD mutations | N | Neural precursor cells, neurons | [37] |
OE, Overexpression; * N, Number of analysed individuals (unrelated, unless stated otherwise), i.e., population size; n, Number of independently-generated iPS clones, i.e., sample size, N = No; Y = Yes; Y/N = Undetermined.