Neurochemical Research

, Volume 32, Issue 9, pp 1483–1488 | Cite as

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

  • Won Kyung Hong
  • Eun Hae Han
  • Dae Ghon Kim
  • Jung Yup Ahn
  • Jeong Soon Park
  • Bok Ghee Han
Original Paper


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.


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


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Copyright information

© Springer Science+Business Media, LLC 2007

Authors and Affiliations

  • Won Kyung Hong
    • 1
  • Eun Hae Han
    • 1
  • Dae Ghon Kim
    • 2
  • Jung Yup Ahn
    • 1
  • Jeong Soon Park
    • 3
  • Bok Ghee Han
    • 1
  1. 1.Biobank for Health Sciences, Center for Genome SciencesNational Institute of Health, Korea Center for Disease Control and Prevention (KCDC)SeoulKorea
  2. 2.Chonbuk National University Medical SchoolJeonjuKorea
  3. 3.Department of Cellular and Structural BiologyUniversity of Texas Health Science CenterSan AntonioUSA

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