additional evidence supporting a potential beneficial protective role for estrogen in AD. Along these lines, a novel study in
transgenic mice was conducted in whichmice were produced
by crossing aromatase knockout mice with APP23 transgenic
mice, a mouse model of AD [188]. The aromatase knockout-
APP23 transgenic crossed mice allowed the investigators to
study the effect of estrogen depletion on A-beta plaque formation
in a well-characterized model of AD. The results revealed
that compared to the APP-23 transgenic control mice, the
estrogen-deficient APP23 transgenic mice exhibited greatly
reduced brain estrogen levels and early-onset and increased
beta amyloid peptide deposition. In contrast, ovariectomized