One possible explanation for the toxicity of amyloid-β (Aβ) in Alzheimer’s disease (AD) is that Aβ generates pathological ion channels giving rise to cellular ionic dyshomeostasis. We have shown that Aβ1-42 oligomers can generate channels although the mechanism of channel gating is completely unknown. Two hypotheses have emerged, the first of which is that all mutant amyloid, producing early onset Alzheimer’s disease, should be associated with functional ion channels. Secondly channel gating might be affected by the action of blocking molecules, or hydrogen ion binding at sites in the channel pore, as a required opening step.
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