Amyloid precursor protein increases cortical neuron size in transgenic mice

Esther S. Oh, Alena V. Savonenko, Julie F. King, Stina M. Fangmark Tucker, Gay L. Rudow, Guilian Xu, David R. Borchelt, Juan C. Troncoso

Research output: Contribution to journalArticle


The amyloid precursor protein (APP) is the source of β-amyloid, a pivotal peptide in the pathogenesis of Alzheimer's disease (AD). This study examines the possible effect of APP transgene expression on neuronal size by measuring the volumes of cortical neurons (μm3) in transgenic mouse models with familial AD Swedish mutation (APPswe), with or without mutated presenilin1 (PS1dE9), as well as in mice carrying wild-type APP (APPwt). Overexpression of APPswe and APPwt protein, but not of PS1dE9 alone, resulted in a greater percentage of medium-sized neurons and a proportionate decrease in the percentage of small-sized neurons. Our observations indicate that the overexpression of mutant (APPswe) or wild-type APP in transgenic mice is necessary and sufficient for hypertrophy of cortical neurons. This is highly suggestive of a neurotrophic effect and also raises the possibility that the lack of neuronal loss in transgenic mouse models of AD may be attributed to overexpression of APP.

Original languageEnglish (US)
Pages (from-to)1238-1244
Number of pages7
JournalNeurobiology of Aging
Issue number8
StatePublished - Aug 1 2009


  • Amyloid precursor protein
  • Neuron size
  • Stereology
  • Transgenic mouse models of Alzheimer's disease

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology

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