Figure 1.
Lack of murine apoE dramatically reduces the amount of Aβ/amyloid burden even in very old transgenic mice. Numerous thioflavine S-fluorescent (A) as well as Aβ immunoreactive deposits (C) are evident in both the cortex and hippocampus
of transgenic mice that express the V717F mutant of the amyloid precursor protein as well as apoE, but is dramatically reduced
when apoE is absent (B, D). Adapted from (42).