Table 1.

Research models used for Alzheimer’s disease.

Type	Model	Key Findings	Ref.
2D in vitro models	hESC-derived neurons overexpressing PSEN1	Increased Aβ42/40 ratio due to depletion of Aβ40	[125]
	APP K724N mutated neurons from AD patients	Increased Aβ42/40 ratio due to depletion of Aβ40 and increased secretion of Aβ42	[126]
	hiPSC-derived astrocytes	Increased Aβ42/40 ratio in astrocytes is an important regulator of AD	[127]
	PSEN1 ΔE9 mutated hiPSC-derived astrocytes	Increased Aβ42/40 ratio, ROS, increased cytokine release	[128]
	PSEN1 M146L mutated hiPSC-derived astrocytes	Disturbed expression of astrocyte markers	[129]
	hiPSCs-derived neurons with PSEN1 A246E mutation	Defective mitochondria have a key role in AD	[130]
	ReN immortalized stem cell line	Mutations in APP gene show accumulation of Aβ and phosphorylated tau	[131]
	PC12 immortalized cell line	GLP-1 neuroprotection and findings of Aβ toxicity	[132]
3D in vitro models	PSEN1 A246E iPSC-derived neurons	Aβ aggregation without synthetic Aβ exposure or mutation induction	[133]
	iPSC-derived NPCs encapsulated in wet electrospun PLGA	Enhanced expression of Aβ42 and p-Tau	[134]
	NSCs encapsulated in starPEG-heparin-based hydrogels	Increased Aβ42 causes loss of neuroplasticity. System could allow for identification of therapeutic targets	[135]
	Induced NSCs in silk protein scaffold with HSV-1-induced AD	Aβ plaque formation, neuroinflammation, decreased functionality	[136]
	iPSCs-derived neuro-spheroids	Aβ aggregation; platform for testing of AD drugs	[137]
	3D human neural progenitor cells	Show the importance of reducing the Aβ42/40 ratio for amelioration of AD; accurate tau pathology	[138]
	Acoustofluidic platform for assembly of neurospheroids and Aβ plaques	High throughput screening platform to test drugs against Aβ plaques	[139]
	3D triculture of neurons, astrocytes, and microglial cells	Aβ aggregation, accumulation of p-tau, cytokine secretion	[140]
In vivo models	APP overexpressing mice	Aβ plaque formation, learning, and cognitive deficits after 6 months	[141]
	Aβ-GFP transgenic mice	Aβ is only able to form oligomers, thereby representing AD. Mice showed loss of memory, spine alterations, and increased p-tau levels.	[142]
	hTauP301L transgenic mice	Increased levels of phosphorylated tau, increased tau aggregation, neuronal loss	[143]
	T40PL-GFP transgenic mice, with the P301L 2N4R tau mutation	Increased levels of tau aggregation and tau pathology after 3 months	[144]
	ICV injection of Aβ oligomers	Memory loss in an ERK1/2-mediated fashion	[145]