Accelerated Aβ deposition in APPswe/PS1ΔE9 mice with hemizygous deletions of TTR (transthyretin)

Hoon Choi Se, Susan N. Leight, Virginia M.Y. Lee, Tong Li, Philip C. Wong, Jeffrey A. Johnson, Maria J. Saraiva, Sangram S. Sisodia

Research output: Contribution to journalArticlepeer-review

106 Scopus citations


A cardinal pathological lesion of Alzheimer's disease (AD) is the deposition of amyloid β (Aβ) in the brain. We previously reported that exposing transgenic mice harboring APPswe/PS1ΔE9 transgenes to an enriched environment resulted in reduced levels of Aβ peptides and deposition, findings that were correlated with an increase in the expression of TTR, encoding transthyretin (TTR). TTR is expressed at high levels in the choroid plexus and known to bind Aβ peptides and modulate their aggregation in vitro and in vivo. To explore the impact of TTR expression on Aβ levels and deposition in vivo, we crossed ceAPPswe/PS1ΔE9 transgenic mice to mice with genetic ablations of TTR. We now report that the levels of detergent-soluble and formic acid-soluble levels of Aβ and deposition are elevated in the brains of ceAPPswe/PS1ΔE9/TTR+/- mice compared with age-matched ceAPPswe/PS1ΔE9/TTR+/+ mice. Moreover, Aβ deposition is significantly accelerated in the hippocampus and cortex of ceAPPswe/ PS1ΔE9/TTR+/- mice. Our results strongly suggest that TTR plays a critical role in modulating Aβ deposition in vivo.

Original languageEnglish (US)
Pages (from-to)7006-7010
Number of pages5
JournalJournal of Neuroscience
Issue number26
StatePublished - Jun 27 2007


  • Alzheimer's disease
  • Amyloid
  • Aβ peptide
  • Presenilin 1
  • Transgenic mice
  • Transthyretin

ASJC Scopus subject areas

  • General Neuroscience


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