TABLE 1.
An overview of the pathological changes of different pre-clinical models of AD (Hsiao et al., 1996; Hsia et al., 1999; Dudal et al., 2004; Jankowsky et al., 2004; Grootendorst et al., 2005; Radde et al., 2006; Minkeviciene et al., 2009; Tai et al., 2011; Yue et al., 2011; Jawhar et al., 2012; Kamphuis et al., 2012; Cohen et al., 2013; Granger et al., 2016; Myers and McGonigle, 2019).
| Models of AD | Genetic background |
Mutations |
Development (months) |
|||||
| APP | PSEN1 | Plaque | Tangles | Gliosis | Memory deficit | |||
| 5xFAD | Mixed: C57BL/6 and SJL | Swedish: K670N/M671L Florida: I716V London: V717I | M146L L286V | 1.5 | ND | 1 | 4 | |
| C57BL/6J | 2 | ND | 2 | 3 | ||||
| APP/PS1 | C57BL/6J | Swedish: K595N/M596L | L166P | 3–4 | NMT | 1.5 | 7 | |
| APPswe/PSEN1Δ E9 | C57BL/6J | Swedish: K670N/M671L | deltaE9 | 9 | NMT | 6 | 12 | |
| PSAPP | C57BL/6J* or Mixed: C57BL/6 and C3H | Swedish: K670N/M671L | M146L | 6 | 6 | 6 | 3 | |
| PDGF-APPSw, Ind J9 | C57BL/6J | Swedish: K670N/M671L Indiana: V717F | 21–25 | NMT | ND | ND | ||
| PDGF-APPSw, Ind J20 | C57BL/6J | Swedish: K670N/M671L Indiana: V717F | 7–8 | Absent | 6 | 4 | ||
| Tg2576 | C57Bl/SJL | Swedish: K670N/M671L | 11–13 | Absent | 10–16 | 6–12 | ||
| TgCRND8 | C57Bl/6 | Swedish: K670N/M671LIndiana: V717F | 3 | Absent | 4 | 3 | ||
| TgF344 | Fischer 344 | Swedish: K670N/M671L | deltaE9 | 6 | 16 | 6 | 15 | |
| Models of AD | Strain background | Other mutations | Plaque | Tangles | Gliosis | Memory deficits | ||
| APOE3-TR | C57BL/6J | Apoe replaced with human APOE3 | 10 (few) | ND | ND | ND | ||
| APOE4-TR | C57BL/6J | Apoe replaced with human APOE4 | 10 (few) | ND | ND | 4–5 | ||
| rTg4510 | Mixed: 129S6 and FVB | Human tau MAPTP301L | Absent | 2.5 | 2.5 | 2.5 | ||
app, amyloid precursor protein; psen1, presenilin 1; ND, no data; NMT, no mature tangles. *PSAPP mice bred on C57BL/6J have a seizure phenotype.