Table 3.

Common transgenic mouse models of AD utilized in metabolomics studies.

Model	Transgene/mutation	Phenotype	Reference
APP (Tg2576)	APP: KM670/671NL (Swedish)	5- and 14-fold increase of Aβ40 and Aβ42/43, respectively Aβ plaques by 11 months Gliosis identified near Aβ plaques by 10 months Cognitive impairment detected by 3–6 months	(114, 115)
PS1 (line 5.1)	PSEN1: M146L	2- to 3-fold increase of mutant PSEN1 Elevated Aβ42/43 in the brain	(116)
APP/PS1	APP: KM670/671NL (Swedish) PSEN1: M146L	Enhanced pathology compared to single transgene Aβ deposits by 6 months Gliosis by 6 months Cognitive impairment detected by 3 months	(117, 118)
3xTg	APP: KM670/671NL (Swedish) PSEN1: M146V MAPT: P301L	Age-associated pathology Aβ deposits by 6 months Tau pathology by 12 months Gliosis by 7 months Cognitive impairment detected by 4 months	(119–121)
5xFAD	APP: KM670/671NL (Swedish); I716V (Florida); V717I (London) PSEN1: M146L; L286V	Early and aggressive presentation Aβ deposits by 1.5 months Gliosis by 2 months Cognitive impairment detected by 4 months	(122, 123)
APOE4	APOE4 targeted replacement	APOE levels and plasma lipids in ε4 mice do not differ significantly to ε3 mice APOE4 mice have reduced VLDL clearance rate compared to APOE3 mice	(124)
EFAD	5xFAD with APOE (2, 3, or 4) knock-in	APOE4 mice (E4FAD) have increased plaques compared to E3FAD and E2FAD models Plaque formation between 4 and 6 months Gliosis at 6 months of age in all models Cognitive decline in E4FAD > E3/E2FAD	(125)

APOE, apolipoprotein E; APP, amyloid precursor protein; FAD, familial Alzheimer’s disease; MAPT, microtubule-associated protein tau; PS1/PSEN1, presenilin-1; VLDL, very low density lipoprotein.