Table 2.
APOE in Aβ transgenic models. Genetic deletion of mouse apoE (apoE−/−) from Aβ-Tg mice delays amyloid deposition, which is further delayed by the introduction of h-APOE into Aβ-Tg mice. *LaDu Lab unpublished observations.
| Aβ pathology (age of onset) | ||||||
|---|---|---|---|---|---|---|
| Transgenic line | 2–4 months | 4–8 months | 8–10 months | 11–13 months | ≥13 months | Total Aβ levels |
| PDAPP+/− [36–39] |
Diffuse Aβ
staining: hippocampus cortex |
ThioS (moderate): hippocampus cortex |
ThioS (heavy): hippocampus cortex |
ThioS (heavier): hippocampus cortex |
||
| PDAPP+/− × apoE+/− [40] |
ThioS (low): hippocampus cortex |
ThioS (moderate): hippocampus cortex |
||||
| PDAPP+/− × apoE−/−[41] |
Diffuse Aβ
staining:
hippocampus |
Thios (low):
hippocampus cortex |
6, 12, 15, 18, and 21 months:
PDAPP+/− > PDAPP+/−/apoE−/− |
|||
| PDAPP+/− × GFAP-apoE+/− [42] |
Thios (moderate):
hippocampus E4 > E3 > E2 |
6, 12, 15, 18, and 21 months:
E4 > E3 |
||||
| PDAPP+/+ × apoE-TR [43] |
ThioS low:
hippocampus E4 > E3 = E2 cortex E4 > E3 > E2 |
3 and 12 months:
E4 > E3 |
||||
|
| ||||||
| Tg2576 [42, 44–46] |
Thios (low):
hippocampus cortex |
ThioS (moderate):
hippocampus cortex |
ThioS (heavy):
hippocampus cortex |
|||
|
CAA-fibrillar (low):
leptomeningeal and cortical vessels |
CAA-fibrillar (heavy):
leptomeningeal and cortical vessels |
CAA-fibrillar (heavy):
leptomeningeal and cortical vessels |
||||
| Tg2576 × apoE−/− [42] |
Diffuse Aβ
staining: hippocampus cortex |
12 months Tg2576 > Tg2576/apoE−/− | ||||
| Tg2576 × apoE-TR[47] |
CAA-fibrillar (moderate):
leptomeningeal vessels E4 > E3 |
|||||
|
| ||||||
| J9 mice [48] |
ThioS (moderate):
cortex hippocampus |
|||||
| J9 X NSE-apoE [26] |
ThioS:
hippocampus E4 > E3 |
|||||
|
| ||||||
| 5xFAD [49] |
ThioS (moderate):
hippocampus cortex |
ThioS (heavy):
hippocampus cortex |
||||
| *5xFAD × apoE-TR [50–53] |
ThioS (low):
hippocampus cortex |
|||||