J Alzheimers Dis. 2004 Aug;6(4):367-77; discussion 443-9. Related Articles,
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Curcumin interaction with copper and iron suggests one possible mechanism of
action in Alzheimer's disease animal models.

Baum L, Ng A.

Department of Medicine and Therapeutics, Chinese University of Hong Kong,
Shatin. lwbaum@cuhk.edu.hk

Curcumin is a polyphenolic diketone from turmeric. Because of its anti-oxidant
and anti-inflammatory effects, it was tested in animal models of Alzheimer's
disease, reducing levels of amyloid and oxidized proteins and preventing
cognitive deficits. An alternative mechanism of these effects is metal
chelation, which may reduce amyloid aggregation or oxidative neurotoxicity.
Metals can induce Abeta aggregation and toxicity, and are concentrated in AD
brain. Chelators desferrioxamine and clioquinol have exhibited anti-AD effects.
Using spectrophotometry, we quantified curcumin affinity for copper, zinc, and
iron ions. Zn2+ showed little binding, but each Cu2+ or Fe2+ ion appeared to
bind at least two curcumin molecules. The interaction of curcumin with copper
reached half-maximum at approximately 3-12 microM copper and exhibited positive
cooperativity, with Kd1 approximately 10-60 microM and Kd2 approximately 1.3
microM (for binding of the first and second curcumin molecules, respectively).
Curcumin-iron interaction reached half-maximum at approximately 2.5-5 microM
iron and exhibited negative cooperativity, with Kd1 approximately 0.5-1.6
microM and Kd2 approximately 50-100 microM. Curcumin and its metabolites can
attain these levels in vivo, suggesting physiological relevance. Since curcumin
more readily binds the redox-active metals iron and copper than redox-inactive
zinc, curcumin might exert a net protective effect against Abeta toxicity or
might suppress inflammatory damage by preventing metal induction of NF-kappaB.

PMID: 15345806 [PubMed - in process]

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