Original Paper

Neurochemical Research

, Volume 32, Issue 9, pp 1483-1488

First online:

Amyloid-β-Peptide Reduces the Expression Level of Mitochondrial Cytochrome Oxidase Subunits

  • Won Kyung HongAffiliated withBiobank for Health Sciences, Center for Genome Sciences, National Institute of Health, Korea Center for Disease Control and Prevention (KCDC)
  • , Eun Hae HanAffiliated withBiobank for Health Sciences, Center for Genome Sciences, National Institute of Health, Korea Center for Disease Control and Prevention (KCDC)
  • , Dae Ghon KimAffiliated withChonbuk National University Medical School
  • , Jung Yup AhnAffiliated withBiobank for Health Sciences, Center for Genome Sciences, National Institute of Health, Korea Center for Disease Control and Prevention (KCDC)
  • , Jeong Soon ParkAffiliated withDepartment of Cellular and Structural Biology, University of Texas Health Science Center
  • , Bok Ghee HanAffiliated withBiobank for Health Sciences, Center for Genome Sciences, National Institute of Health, Korea Center for Disease Control and Prevention (KCDC) Email author 

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Abstract

Mitochondrial dysfunction is an important cause of neurological disorder including Alzheimer’s disease (AD). Mitochondria play a key role in the generation of reactive oxygen species (ROS), resulting in oxidative damage to neuronal cell and cellular compartments in the AD brain. Cytotoxicity induced by amyloid-beta (Aβ), a protein fragment of 25–35 amino acids in amyloid plaques has been shown to have neuro-toxic properties. They seem to involve mitochondrial dysfunction, but the underlying mechanisms are not clearly understood. The purpose of this study was to assess whether Aβ induced mitochondrial dysfunction involves changes in cytochrome c oxidase (COX) expression. We measured the activities of COX after expose of SK-N-SH cells (a human neuroblastoma cell line) to Aβ. We found that levels of mRNAs expressing mitochondrial COX subunits decreased significantly in Aβ-treated SK-N-SH cells in a dose-dependent manner. Human mitochondrial transcription factor-1 (TFAM) mRNA level also decreased after Aβ-treatment. These results suggest that Aβ modulates the mitochondrial gene expression through a decrease in TFAM.

Keywords

Alzheimer’s disease (AD) Amyloid-beta (Aβ) Reactive oxygen species (ROS) Cytochrome oxidase (COX) Human mitochondrial transcription factor-1 (TFAM)