Table 2.

3D iPSC-based Models of AD.

3D iPSC-based Models	Mutation/Genomic alteration	AD hallmarks	Reference (s)
fAD brain organoids/3D matrix	PSEN2 (N141I)	higher Aβ42/Aβ40 ratio, asynchronous calcium transients, enhanced neuronal hyperactivity	[82]
fAD brain organoids	APOE4	Aβ plaques and hyperphosphorylated Tau	[130]
fAD organoids	APP duplication line/ PSEN1 (PSEN1M146I, PSEN1A264E)	higher amyloid aggregation and hyperphosphorylated Tau and endosomal abnormalities	[178]
fAD and Down syndrome-organoids	PSEN1 (PSEN1A264E)	accumulation of structures reminiscent to and trisomy of ch21 (Ts21) amyloid plaques and neurofibrillary tangles	[179]
fAD organoids	APOE4	Aβ deposits, hyperphosphorylated Tau and decreased synaptic integrity	[180]
3D human tri-culture in a	APP	Aβ aggregation, NFT formation, increased pro-inflammatory cytokines microfluidic platform microglial recruitment and neuron/astrocyte loss	[182]
fAD-hippocampal spheroids	APP/PSEN1	increased Ab42/Ab40 peptide ratios and decreased synaptic protein levels	[185]