TABLE 3.

Characteristics of the App knock-in mouse lines.

	Stain	Gene mutations		Genetic background	Aβ plaques (first appearance)	Tangles	Neuronal loss	Cognitive impairment	Strengths	Weaknesses
		App	Psen1
Single App knock-in	App huAβ	Humanized Aβ	–	C57BL/6J	–	NR	NR	NR	A control for other models	–
	AppNL	Humanized Aβ KM670/671NL	–	C57BL/6J	–	–	–	–	A control for other models	No amyloid pathology No cognitive deficits Increased CTF-β
	AppNL–F	Humanized Aβ KM670/671NL I716F	–	C57BL/6J	6 months	–	–	18 months	Deposition of wild type human Aβ	Long time required for amyloid pathology and cognitive deficits Increased CTF-β
	AppNL–G–F	Humanized Aβ KM670/671NL E693G I716F	–	C57BL/6J	2 months	–	–	6 months	Early appearance of amyloid pathology	The Arctic mutation inside the Aβ sequence Increased CTF-β
	AppG–F	Humanized Aβ E693G I716F	–	C57BL/6J	4 months	NR	NR	NR	Absence of the Swedish mutation No increase of CTF-β	The Arctic mutation inside the Aβ sequence
App and Psen1 double mutant	AppNL–F Psen1P117L	Humanized Aβ KM670/671NL I716F	P117L	C57BL/6J	3 months	NR	NR	NR	Early appearance of amyloid pathology Deposition of wild type human Aβ	Mutations in both App and Psen1 genes

The Swedish mutations; KM670/671NL.

The Iberian/Beyreuther mutation; I716F.

The Arctic mutation; E693G.

NR denotes data not reported.