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summary, we demonstrate that abrogating Aβ production halts the progression of pathologic changes in a transgenic mouse model of Alzheimer-type amyloidosis. However, despite dramatic reductions in Aβ synthesis, neuritic plaques are stable structures in vivo that do not quickly disaggregate. It is possible that a combination of therapies to limit Aβ production, increase Aβ degradation, and enhance phagocytosis of deposited amyloid may be required to reverse damage associated with AD. However, if started early enough in the course of disease, secretase inhibitors alone could provide substantial benefit in slowing pathogenic processes linked to amyloid deposition. Even at later stages in the disease, the presence of substantial microglial activation in human AD [40] suggests that simply slowing the formation of new amyloid deposits may allow ongoing phagocytosis to diminish preexisting lesions. However, the development of safe and effective secretase inhibitors will ultimately be required to determine whether the human brain has the capacity to repair amyloid-associated damage of AD once the progression of pathology is arrested."}

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