Table 2. Transgenic mouse models that have cognitive deficit phenotypes

Name Promoter Mutation(s) Symptoms Refs
Senescence-accelerated mouse prone (SAMP) SAMP8 mice - - Age-associated increase in Aβ deposition in hippocampal from 4 to 12 mon ⟹ Astrogliosis, microgliosis, and cognitive deficits (Takeda et al., 1981)
Single APP knock-in AppNL-G-F mice Endogenous APP APPKM670/671NL, E693G, I716F Aβ plaque deposition observed starting at 2 mon and is nearly saturated by 7 mon ⟹ Gliosis and cognitive deficits (Guerreiro et al., 2010; Mullan et al., 1992; Nilsberth et al., 2001)
Double transgenic APP-Tg × PSEN1-Tg APP/PS1 transgenic mice Mouse Thy1 (APP, PS1) APPKM670/671NL PS1I166P Aβ plaque deposition starting at approximately 6 wk of age in the neocortex ⟹ Astrogliosis, microgliosis, formation of dystrophic neuritis, neuronal loss, and cognitive deficits (Maia et al., 2013; Radde et al., 2006)
5xFAD transgenic mice Mouse Thy1.2 (APP, PS1) APPKM670/671NL, I716V, V717I PS1M146L, L286V Neuron loss occurs in multiple brain regions beginning at 6 mon of age ⟹ Astrogliosis, microgliosis, neuronal loss, and cognitive deficits (Devi and Ohno, 2010; Oakley et al., 2006)
Triple transgenic 3xTg-AD mice Mouse Thy1.2 (APP) Endogenous (PS1) APPK670N, M671L PS1M146V MAPTP301L Aβ deposition with intracellular immunoreactivity detected in some brain regions as early as 3–4 mon of age ⟹ Gliosis and cognitive deficits (Oddo et al., 2003)
Aβ, amyloid beta; APP, amyloid precursor protein; Tg, transgenic; PS1, presenilin-1; Thy, promotor of Thy-1 cell surface antigen gene; FAD, familial Alzheimer’s disease; MAPT, microtubule-associated protein Tau.