Abstract
There is increasing evidence to support a role for both the amyloid β-protein precursor (AβPP) and its proteolytic fragment, amyloid β (Aβ), in metal ion homeostasis. Furthermore, metal ions such as zinc and copper can interact with both AβPP and Aβ to potentiate Alzheimer's disease by participating in the aggregation of these normal cellular proteins and in the generation of reactive oxygen species. In addition, metal ions may interact on several other AD-related pathways, including those involved in neurofibrillary tangle formation, secretase cleavage of AβPP and proteolytic degradation of Aβ. As such, a dysregulation of metal ion homeostasis, as occurs with both aging and in AD, may foster an environment that can both precipitate and accelerate degenerative conditions such as AD. This offers a broad biochemical front for novel therapeutic interventions.
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