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- W3020852512 abstract "By using a BRI–Aβ fusion strategy, we have developed BRI–Aβ transgenic mice that allow selective expression of either Aβ40 or Aβ42 in the secretory pathway without APP overexpression. BRI–Aβ40 mice express high levels of Aβ40, but do not have detectable levels of insoluble Aβ40 and do not develop amyloid deposits at any age. In contrast, BRI–Aβ42 mice expressing Aβ42 develop diffuse and cored parenchymal plaques and congophilic amyloid angiopathy (CAA) from 3 months of age. These results suggest Aβ42, but not Aβ40, plays an essential role in the initiation of amyloid deposition. The purpose of this study was to investigate the effect of altering the ratio of Aβ42/Aβ40 on amyloid deposition and AD–related pathology by crossbreeding the BRI–Aβ40 and BRI–Aβ42 mice and also with mutant APP (Tg2576) transgenic mice. BRI–Aβ42 mice and BRI–Aβ40 were bred with Tg2576 (APP695NL) mice and with each other. An aging series (2–24 month) of bigenic mice and their singly transgenic parental lines were analyzed biochemically, using Aβ40 or Aβ42 end–specific sandwich ELISAs, and pathologically for parenchymal and vascular amyloid deposition using immunohistochemistry techniques for Aβ. (1) At 15 months bigenic BRI–Aβ42/Tg2576 mice had >40 times greater amyloid burden in hippocampus and entorhinal cortex than singly transgenic BRI–Aβ42 and Tg2576 littermates. CAA was also significantly increased in BRI–Aβ42/Tg2576 mice. (2) Although bigenic BRI–Aβ40/Tg2576 mice had higher total levels of soluble Aβ, the BRI–Aβ40/Tg2576 mice had significantly less amyloid deposition in both the parenchyma (80% reduction) and cerebrovasculature (75% decrease) than Tg2576 littermates at 15 months. (3) While singly transgenic BRI–Aβ40 mice had no Aβ40 deposition nor insoluble Aβ40 and BRI–Aβ42 mice only accumulated RIPA–insoluble Aβ42, bigenic BRI–Aβ42/BRI–Aβ40 mice had massive amounts of RIPA–insoluble Aβ40 in both the forebrain (∼1200 pmole/g) and hindbrain (∼ 3600 pmole/g) suggesting that the addition of Aβ42 “seeded” pathology in the bigenic mice. Taken together, these data suggest that Aβ42 functions as a seed for the initiation of amyloid deposition and more importantly the ratio of Aβ42 to Aβ40, rather than the total Aβ level, may determine the extent of parenchymal and vascular Aβ deposition." @default.
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- W3020852512 date "2006-07-01" @default.
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- W3020852512 title "P1-113: The Abeta42/Abeta40 ratio, not total Abeta level, controls amyloid deposition in transgenic mice" @default.
- W3020852512 doi "https://doi.org/10.1016/j.jalz.2006.05.489" @default.
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