Abstract
Over a decade of studies have pointed to metal mediated neural oxidative damage as an attractive target for the treatment of Alzheimers disease. Because of the nature of the blood brain barrier, systemic depletion of the metals, copper, zinc and possibly iron, is not a viable approach. However preliminary studies with CQ, a blood brain barrier penetrating chelating agent, are showing promise. CQ probably works by combining with the metal centres, primarily copper and zinc complexes of Aβ, in the neuropil. This review discusses some of the background that resulted in CQ becoming a lead compound and how we might advance our understanding of its action
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