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Interactions of Npc1 and amyloid accumulation/deposition in the APP/PS1 mouse model of Alzheimer’s

  • Animal Genetics ∙ Original Paper
  • Published:
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Abstract

Although Niemann-Pick C1 disease has frequently been called “juvenile Alzheimer’s”, the effects of introducing Npc1 mutations into a mouse model of Alzheimer’s have not previously been performed. We have crossed Npc1 +/− mice with APP/PS1 “Alzheimer’s” mice and studied Aβ42 accumulation and amyloid plaque formation. Mice heterozygous for Npc1 and positive for the APP and PS1 transgenes accumulated Aβ42 more rapidly than the APP/PS1 controls and this correlated, as expected, with the area of amyloid plaques. We conclude that the alterations of intracellular cholesterol present in Npc1 +/− mice can influence the progress of Alzheimer’s disease in the APP/PS1 mouse model.

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Acknowledgements

This work was supported by NIH, grant number 5RO1 EB000343-05, Dr. Theodore Trouard, P.I. We thank Dr. F. John Meaney for help with statistics, and John Totenhagen for help with image analysis.

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Correspondence to Robert P. Erickson.

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Borbon, I.A., Erickson, R.P. Interactions of Npc1 and amyloid accumulation/deposition in the APP/PS1 mouse model of Alzheimer’s. J Appl Genetics 52, 213–218 (2011). https://doi.org/10.1007/s13353-010-0021-1

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