NDLI: Copper induces the accumulation of amyloid-beta in the brain

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Analysis of mRNA expression profiles highlights alterations in modulation of the DNA damage-related genes under butanal exposure in A549 human alveolar epithelial cells

Molecular & Cellular Toxicology : Volume 8

Molecular & Cellular Toxicology : Volume 7

Molecular & Cellular Toxicology : Volume 6

Copper induces the accumulation of amyloid-beta in the brain

Content Provider	Springer Nature Link
Author	Kim, Dong Kyeong Song, Ji Won Park, Jung Duck Choi, Byung Sun
Copyright Year	2013
Abstract	Accumulation of amyloid beta protein (Aβ) plays a major role in the etiology of Alzheimer’s disease (AD). Aβ is generated from the cleavage of amyloid precursor protein (APP) by beta-site APP-cleaving enzyme 1 (BACE1). There are two factors that reduce of Aβ accumulation in the brain; degradation by peptidases such as neprilysin (NEP) and clearance via two transporters. The low-density lipoprotein receptor related protein 1 (LRP1) is the major transporter that clears Aβ from brain to blood and the receptor for advanced glycation end products (RAGE) is a receptor that transports Aβ from blood to brain. Copper (Cu) has been postulated to play a role in the pathogenesis of AD, especially involved in Aβ aggregation and toxicity. According to a recent study, Cu(II) could reduce Aβ clearance from the brain in cholesterol-fed rabbits. However, the critical mechanism is unclear. This study was purposed to demonstrate whether Cu (II) would alter accumulation of Aβ in brain. We treated 25 and 50 μM CuSO$_{4}$ for 48-hour in the well-defined neurodevelopmental cell line (PC12), rat choroidal epithelial cell line (Z310), and rat brain endothelial cell line (RBE4) to estimate the effects on Cu(II) exposure in the brain.Cu(II) increased the levels of Aβ(40) and Aβ(42) in the PC12 cell medium in a dose-dependent manner compared with control. The mRNA and protein expression levels of APP and BACE1, which play an important role in Aβ generation, were increased in the PC12 cells exposed to Cu(II). NEP expression levels in mRNA and protein were decreased in a dose-dependent manner in PC12 cells treated with Cu(II). In the RBE4 cells, Cu(II) decreased LRP1 levels and increased RAGE levels in mRNA and protein compared with control. Moreover, Cu(II) decreased the clearance of Aβ using the blood-brain barrier (BBB) transport study. However, in the Z310 cells, Cu(II) didn’t change the levels of LRP1 and RAGE in mRNA and protein. These results implied that Cu(II) increased Aβ accumulation in the brain by increasing Aβ production but decreasing Aβ degradation in the brain parenchyma and interfering with clearance of Aβ via the BBB.
Starting Page	57
Ending Page	66
Page Count	10
File Format	PDF
ISSN	1738642X
Journal	Molecular & Cellular Toxicology
Volume Number	9
Issue Number	1
e-ISSN	20928467
Language	English
Publisher	The Korean Society of Toxicogenomics and Toxicoproteomics
Publisher Date	2013-04-03
Publisher Place	Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Amyloid beta protein Amyloid precursor protein (APP) Beta-site APP-cleaving enzyme 1 (BACE1) Blood-brain barrier (BBB) Blood-CSF barrier (BCB) Copper Neprilysin (NEP) Low-density lipoprotein receptor related protein 1 (LRP1) Receptor for advanced glycation end products (RAGE) Cell Biology Pharmacology/Toxicology
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Public Health, Environmental and Occupational Health Toxicology Pathology and Forensic Medicine

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