Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease

Monica Garcia-Alloza, Elissa M. Robbins, Sandy X. Zhang-Nunes, Susan M. Purcell, Rebecca A. Betensky, Susan Raju, Claudia Prada, Steven M. Greenberg, Brian J. Bacskai, Matthew P. Frosch

Research output: Contribution to journalArticlepeer-review


Transgenic mice carrying disease-linked forms of genes associated with Alzheimer disease often demonstrate deposition of the β-amyloid as senile plaques and cerebral amyloid angiopathy. We have characterized the natural history of β-amyloid deposition in APPswe/PS1dE9 mice, a particularly aggressive transgenic mouse model generated with mutant transgenes for APP (APPswe: KM594/5NL) and PS1 (dE9: deletion of exon 9). Ex vivo histochemistry showed Aβ deposition by 4 months with a progressive increase in plaque number up to 12 months and a similar increase of Aβ levels. In vivo multiphoton microscopy at weekly intervals showed increasing β-amyloid deposition as CAA and plaques. Although first appearing at an early age, CAA progressed at a significantly slower rate than in the Tg2576 mice. The consistent and early onset of β-amyloid accumulation in the APPswe/PS1dE9 model confirms its utility for studies of biochemical and pathological mechanisms underlying β-amyloid deposition, as well as exploring new therapeutic treatments.

Original languageEnglish (US)
Pages (from-to)516-524
Number of pages9
JournalNeurobiology of Disease
Issue number3
StatePublished - Dec 2006


  • APPswe/PS1dE9
  • Alzheimer disease
  • Amyloid-β
  • Cerebral amyloid angiopathy
  • Transgenic mouse

ASJC Scopus subject areas

  • Neurology


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