Neuron loss in APP transgenic mice

Michael E. Calhoun, Karl-Heinz Wiederhold, Dorothee Abramowski, Amie L. Phinney, Alphonse Probst, Christine Sturchler-Pierrat, Matthias Staufenbiel, Bernd Sommer and Mathias Jucker ()
Additional contact information
Michael E. Calhoun: Neuropathology, Institute for Pathology, University of Basel
Karl-Heinz Wiederhold: Novartis Pharma Ltd, Nervous System Research
Dorothee Abramowski: Novartis Pharma Ltd, Nervous System Research
Amie L. Phinney: Neuropathology, Institute for Pathology, University of Basel
Alphonse Probst: Neuropathology, Institute for Pathology, University of Basel
Christine Sturchler-Pierrat: Novartis Pharma Ltd, Nervous System Research
Matthias Staufenbiel: Novartis Pharma Ltd, Nervous System Research
Bernd Sommer: Novartis Pharma Ltd, Nervous System Research
Mathias Jucker: Neuropathology, Institute for Pathology, University of Basel

Nature, 1998, vol. 395, issue 6704, 755-756

Abstract: Abstract Alzheimer's disease (AD) is a progressive neurodegenerative disorder that affects a large proportion of the elderly population. Amyloid plaques, which are a neuro-pathological characteristic of AD, have been reproduced in transgenic mice by the overexpression of mutant forms of the amyloid-β precursor protein (APP) known to cause familial AD. Here we report that these mice exhibit selective neuronal death in the brain regions that are most affected in AD, suggesting that amyloid plaque formation is directly involved in AD neuron loss.

Date: 1998
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DOI: 10.1038/27351

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