Journal article

Zinc and copper modulate Alzheimer Aβ levels in human cerebrospinal fluid

D Strozyk, LJ Launer, PA Adlard, RA Cherny, A Tsatsanis, I Volitakis, K Blennow, H Petrovitch, LR White, AI Bush

Neurobiology of Aging | Published : 2009

Abstract

Abnormal interaction of β-amyloid 42 (Aβ42) with copper, zinc and iron induce peptide aggregation and oxidation in Alzheimer's disease (AD). However, in health, Aβ degradation is mediated by extracellular metalloproteinases, neprilysin, insulin degrading enzyme (IDE) and matrix metalloproteinases. We investigated the relationship between levels of Aβ and biological metals in CSF. We assayed CSF copper, zinc, other metals and Aβ42 in ventricular autopsy samples of Japanese American men (N = 131) from the population-based Honolulu Asia Aging Study. There was a significant inverse correlation of CSF Aβ42 with copper, zinc, iron, manganese and chromium. The association was particularly strong in..

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University of Melbourne Researchers

Grants

Awarded by Australian Research Council


Funding Acknowledgements

This study was supported by NIH (National Institute on Aging); Grant Numbers 1RO1 AG12686 (to AIB), 1 U01 AG19349-01, 5 R01 AG017155-04, and in part by the Intramural Research Program of the NIH, National Institute on Aging, as well as (to AIB) the Australian Research Council Federation Fellowship, the National health and Medical Research Council of Australia, the Alzheimer Association Zenith Award and the American Health Assistance Foundation. The Victorian Brain Bank Network is supported by The University of Melbourne, The Mental Health Research Institute of Victoria, Victorian Forensic Institute of Medicine and funded by Neurosciences Australia and the National Health & Medical Research Council.