Role of Intracellular Aß42 in AD
Intracellular Aß aggregates might also impair normal neuronal function even in the absence of overt pathological change. (see diagram)
- There are now several reports that behavioral change occurs in the absence of overt pathology in transgenic mice overexpressing wild type APP (as occurs in human trisomy 21) or the mutant APP genes that cause familial AD.
- It should now be possible to test the hypothesis that these behaviors are related to changes in intracellular Aß that are relevant to human AD, where plaque formation may occur more readily than in mice.