Mj. Callahan et al., Augmented senile plaque load in aged female beta-amyloid precursor protein-transgenic mice, AM J PATH, 158(3), 2001, pp. 1173-1177
Citations number
33
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Transgenic mice (Tg2576) overexpressing human beta -amyloid precursor prote
in with the Swedish mutation (APP695SWE) develop Alzheimer's disease-like a
myloid beta protein (A beta) deposits by 8 to 10 months of age. These mice
show elevated levels of A beta 40 and A beta 42, as well as an age-related
increase in diffuse and compact senile plaques in the brain. Senile plaque
load was quantitated in the hippocampus and neocortex of 8- to 19-month-old
male and female Tg2576 mice. In all mice, plaque burden increased markedly
after the age of 12 months. At 15 and 19 months of age, senile plaque load
was significantly greater in females than in males; in 31 mice studied at
15 months of age, the area occupied by plaques in female Tg2576 mice was ne
arly three times that of males. By enzyme-linked immunosorbent assay, femal
e mice also had more A beta 40 and A beta 42 in the brain than did males, a
lthough this difference was less pronounced than the difference in histolog
ical plaque load. These data show that senescent female Tg2576 mice deposit
more amyloid in the brain than do male mice, and may provide an animal mod
el in which the influence of sex differences on cerebral amyloid pathology
can be evaluated.