Table 4 Cellular models of Alzheimer’s disease

iPSC (patient-derived induced pluripotent stem cells)

FAD or SAD

Yes, Aβ42 and APP levels increase 42 days past differentiation in FAD and SAD cell lines.

Yes, elevated phosphorylation observed at 42 days post differential date.

Peak at 52 to 70 days after differentiation.

Potentially

No

[194]

[195]

Brain organoids from patient-derived iPSCs

FAD or SAD

Yes, 12 days after serum treatment in SAD models.

Yes, it is present in FAD genetic mutation organoids.

Yes, 12 days after serum treatment SAD models.

Yes, it is present in the FAD genetic mutation organoids.

In APOE and APP/PSEN1 organoids there is a decrease in synaptic integrity.

Yes, in serum-treated SAD models.

APOE4 increases neurodegeneration in iPSC-derived organoids, especially in deeper layers.

[191]

[193]

Patient-derived iNs (direct reprogrammed induced neurons)

FAD or SAD

Yes, Aβ42 levels increase in FAD INs.

APOE4 genotype treated with APP.

FAD fibroblasts do not show elevated levels of tau.

APOE4 genotype treated with APP.

Potentially

No

[181, 182, 184, 185, 196]

Brain organoids from patient-derived iNs

FAD or SAD

Yes, in FAD models with APP and PSEN1 mutations.

SAD models show increased Aβ deposition.

Yes, in FAD models there is an increase in phosphorylated tau and spherical beads in neurites.

SAD models show increase of phosphorylated tau.

SAD models show impairment in synaptic formation.

FAD models have increased cell death compared to healthy controls.

SAD models show neuronal loss and neurite deposition in cortical neurons.

[192]