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To the Editor:
I read with interest the article by Squitti et al.1 I am uncertain of the significance of the non-ceruloplasmin bound copper in the serum of Alzheimer patients. Is it simply a consequence of Alzheimer disease (AD) activity or is directly implicated in the disease process?
AD appears to have free copper unbound by ceruloplasmin in increased amounts. This may have clinical implications since treatment with clioquinol, a metal-protein-attenuating compound which inhibits zinc and copper ions from binding to Abeta and promotes Abeta dissolution, resulted in minimal deterioration of cognitive scores in treated patients compared to substantial deterioration in patients treated with placebo.2
Depleted copper levels have been noted to reduce APP production in animals and it is …
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