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

Artikel i vetenskaplig tidskrift
Författare Dorothea Strozyk
Lenore J Launer
Paul A Adlard
Robert A Cherny
Andrew Tsatsanis
Irene Volitakis
Kaj Blennow
Helen Petrovitch
Lon R White
Ashley I Bush
Publicerad i Neurobiology of aging
Volym 30
Nummer/häfte 7
Sidor 1069-77
ISSN 1558-1497
Publiceringsår 2009
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 1069-77
Språk en
Länkar dx.doi.org/10.1016/j.neurobiolaging...
Ämnesord Aged, Aged, 80 and over, Alzheimer Disease, cerebrospinal fluid, physiopathology, Amyloid beta-Protein, analysis, cerebrospinal fluid, Asian Americans, Brain, metabolism, physiopathology, Brain Chemistry, physiology, Cerebrospinal Fluid, metabolism, Chromium, analysis, cerebrospinal fluid, Cohort Studies, Copper, analysis, cerebrospinal fluid, Humans, Iron, analysis, cerebrospinal fluid, Male, Manganese, analysis, cerebrospinal fluid, Peptide Fragments, analysis, cerebrospinal fluid, Zinc, analysis, cerebrospinal fluid
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

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.

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