Abstract
There is increasing evidence to support a role for both the amyloid beta-protein precursor (AbetaPP) and its proteolytic fragment, amyloid beta (Abeta), in metal ion homeostasis. Furthermore, metal ions such as zinc and copper can interact with both AbetaPP and Abeta 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 AbetaPP and proteolytic degradation of Abeta. 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.
Highlights
Research into the role of metals in Alzheimer’s disease (AD) has rapidly advanced over the past two decades
Studies described controversial links between trace metals and dementia. This concept has developed further with the understanding that a range of biometals and environmental metal toxins are likely to have a central role in determining the onset, progression, and clinical outcomes of Alzheimer’s disease (AD) and other forms of neurodegeneration
Key studies were instigated in the early 1990s by Ashley Bush and colleagues, demonstrating that metals such as zinc and copper were critical in amyloid beta (Aβ) aggregation andtoxicity
Summary
Research into the role of metals in Alzheimer’s disease (AD) has rapidly advanced over the past two decades.
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