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The value of incomplete mouse models of Alzheimer’s disease

European Journal of Nuclear Medicine and Molecular Imaging volume 35, pages 70–74 (2008)Cite this article

Abstract

To study Alzheimer’s disease (AD), a variety of mouse models has been generated through the overexpression of the amyloid precursor protein and/or the presenilins harboring one or several mutations found in familial AD. With aging, these mice develop several lesions similar to those of AD, including diffuse and neuritic amyloid deposits, cerebral amyloid angiopathy, dystrophic neurites and synapses, and amyloid-associated neuroinflammation. Other characteristics of AD, such as neurofibrillary tangles and nerve cell loss, are not satisfactorily reproduced in these models. Mouse models that recapitulate only specific aspects of AD pathogenesis are of great advantage when deciphering the complexity of the disease and can contribute substantially to diagnostic and therapeutic innovations. Incomplete mouse models have been key to the development of Aβ42-targeted therapies, as well as to the current understanding of the interrelationship between cerebral β-amyloidosis and tau neurofibrillary lesions, and are currently being used to develop novel diagnostic agents for in vivo imaging.

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Acknowledgements

We would like to thank Paul Mathews (NKI, Orangeburg, NY, USA) for comments to this manuscript and Tristan Bolmont (Hertie Institute, Tübingen, Germany) for experimental help.

Conflicts of interest

None.

Author information

Affiliations

  1. Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Otfried-Müller Str. 27, D-72076, Tübingen, Germany

    Rebecca Radde, Cecilia Duma & Mathias Jucker

  2. Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge, CB2 0QH, UK

    Michel Goedert

Authors
  1. Rebecca Radde
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  2. Cecilia Duma
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  3. Michel Goedert
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  4. Mathias Jucker
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Corresponding authors

Correspondence to Rebecca Radde or Mathias Jucker.

Additional information

This work was supported by grants to M. J. from the FSP des Landes Baden-Wuerttemberg (Az. 23-7532.22/60), from the BMBF (ARREST-AD and NGFN2), the German Competence Network in Degenerative Dementias (BMBF-01GI0705), and a stipend to C. D. from the Hertie Foundation, Frankfurt, Germany.

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Radde, R., Duma, C., Goedert, M. et al. The value of incomplete mouse models of Alzheimer’s disease. Eur J Nucl Med Mol Imaging 35, 70–74 (2008). https://doi.org/10.1007/s00259-007-0704-y

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  • DOI: https://doi.org/10.1007/s00259-007-0704-y

Keywords

  • Alzheimer’s disease
  • Incomplete mouse model
  • Transgenic mouse models
  • Amyloid
  • Tau