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Zinc and copper modulate Alzheimer Abeta levels in human cerebrospinal fluid.

Abstract：

:Abnormal interaction of beta-amyloid 42 (Abeta42) with copper, zinc and iron induce peptide aggregation and oxidation in Alzheimer's disease (AD). However, in health, Abeta degradation is mediated by extracellular metalloproteinases, neprilysin, insulin degrading enzyme (IDE) and matrix metalloproteinases. We investigated the relationship between levels of Abeta and biological metals in CSF. We assayed CSF copper, zinc, other metals and Abeta42 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 Abeta42 with copper, zinc, iron, manganese and chromium. The association was particularly strong in the subgroup with high levels of both zinc and copper. Selenium and aluminum levels were not associated to CSF Abeta42. In vitro, the degradation of synthetic Abeta substrate added to CSF was markedly accelerated by low levels (2microM) of exogenous zinc and copper. While excessive interaction with copper and zinc may induce neocortical Abeta precipitation in AD, soluble Abeta degradation is normally promoted by physiological copper and zinc concentrations.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

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

doi

10.1016/j.neurobiolaging.2007.10.012

subject

Has Abstract

pub_date

2009-07-01 00:00:00

pages

1069-77

issue

7

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(07)00414-9

journal_volume

30

pub_type

杂志文章

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