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Updated: Jun 21, 2026

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells
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Increased lipid peroxidation in Down's syndrome mouse models.

Keiichi Ishihara1, Kenji Amano, Eiichi Takaki

  • 1Laboratory for Neurogenetics, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan.

Journal of Neurochemistry
|August 4, 2009
PubMed
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Oxidative stress markers, like lipid peroxidation, are elevated in mouse models of Down

Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Down's syndrome (DS) is associated with elevated oxidative stress.
  • Previous studies showed increased oxidative stress in cultured DS cells.
  • In vivo evidence for increased oxidative stress in DS mouse models was lacking.

Purpose of the Study:

  • To investigate in vivo oxidative stress and lipid peroxidation in DS mouse models.
  • To identify proteins affected by oxidative stress in DS brains.
  • To understand the contribution of oxidative stress to DS features.

Main Methods:

  • Examined lipid peroxidation markers (13-HODEs, 4-HNE) in Ts1Cje and Ts2Cje mouse brains.
  • Used oxidation-sensitive fluorescent probes to detect reactive oxygen species (ROS).

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  • Employed electron spin resonance (ESR) to assess antioxidant activity.
  • Utilized mass spectrometry-based proteomics to identify modified proteins.

    • Main Results:

    • Marked increases in protein modifications by 13-HODEs and 4-HNE were observed in Ts1Cje and Ts2Cje brains.
    • Elevated reactive oxygen species (ROS) were detected in Ts1Cje brains.
    • Antioxidant activity in Ts1Cje hippocampus remained unaffected, suggesting accelerated ROS production.
    • Proteomics identified proteins involved in ATP generation, neuronal cytoskeleton, and antioxidant activity as targets of modification.

    Conclusions:

    • In vivo evidence confirms increased oxidative stress and lipid peroxidation in DS mouse models.
    • Oxidative modification of key proteins may impair neuronal function and contribute to DS-related cognitive impairment.
    • Findings highlight the role of accelerated ROS production in the pathophysiology of Down's syndrome.