Treatment with a copper-zinc chelator markedly and rapidly inhibits beta-amyloid accumulation in Alzheimer's disease transgenic mice

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Inhibition of neocortical beta -amyloid (A beta) accumulation may be essential in an effective therapeutic intervention for Alzheimer's disease (AD). Cu and Zn are enriched in A beta deposits in AD, which are solubilized by Cu/Zn-selective chelators in vitro. Here we report a 49% decrease in brain A beta deposition (-375 mug/g wet weight, p = 0.0001) in a blinded study of APP2576 transgenic mice treated orally for 9 weeks with clioquinol, an antibiotic and bioavailable Cu/Zn chelator. This was accompanied by a modest increase in soluble A beta (1.45% of total cerebral A beta); APP, synaptophysin, and GFAP levels were unaffected. General health and body weight parameters were significantly more stable in the treated animals. These results support targeting the interactions of Cu and Zn with A beta as a novel therapy for the prevention and treatment of AD.
Publisher
CELL PRESS
Issue Date
2001-06
Language
English
Article Type
Article
Keywords

A-BETA; MOUSE MODEL; FREE-RADICALS; PEPTIDE; PLAQUES; PROTEIN; AGGREGATION; CLIOQUINOL; PATHOLOGY; BRAINS

Citation

NEURON, v.30, no.3, pp.665 - 676

ISSN
0896-6273
DOI
10.1016/S0896-6273(01)00317-8
URI
http://hdl.handle.net/10203/83617
Appears in Collection
BS-Journal Papers(저널논문)
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