Applied Microscopy

Korean Society of Microscopy (한국현미경학회)
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Ultrastructural Abnormalities in APP/PSEN1 Transgenic Mouse Brain as the Alzheimer's Disease Model

  • Kim, Mi Jeong (Division of Electron Microscopic Research, Korea Basic Science Institute) ;
  • Huh, Yang Hoon (Division of Electron Microscopic Research, Korea Basic Science Institute) ;
  • Choi, Ki Ju (Division of Electron Microscopic Research, Korea Basic Science Institute) ;
  • Jun, Sangmi (Division of Electron Microscopic Research, Korea Basic Science Institute) ;
  • Je, A Reum (Division of Electron Microscopic Research, Korea Basic Science Institute) ;
  • Chae, Heesu (Division of Electron Microscopic Research, Korea Basic Science Institute) ;
  • Lee, Chulhyun (Division of Magnetic Resonance Research, Korea Basic Science Institute) ;
  • Kweon, Hee-Seok (Division of Electron Microscopic Research, Korea Basic Science Institute)
  • Received : 2012.10.27
  • Accepted : 2012.11.19
  • Published : 2012.12.31
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Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder. Neuropathological hallmarks of AD are amyloid plaques, dystrophic neurite, and alteration of subcellular organelles. However, the morpho-functional study of this degenerative process and ultimate neuronal death remains poorly elucidated. In this study, immunohistochemical and ultrastructural analyses were performed to clarify the abnormal morphological alterations caused by the progression of AD in APP/PSEN1 transgenic mice, express human amyloid precursor protein, as a model for AD. In transgenic AD mice brain, the accumulation of Amyloid ${\beta}$ plaques and well-developed dystrophic neurites containing anti-LC3 antibody-positive autophagosomes were detected in the hippocampus and cortex regions. We also found severe disruption of mitochondrial cristae using high-voltage electron microscopy and three-dimensional electron tomography (3D tomography). These results provide morpho-functional evidence on the alteration of subcellular organelles in AD and may help in the investigation of the pathogenesis of AD.

Keywords

References

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