Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin).

Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin). Research Abstract Details 

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Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin). Abstract Text:

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

A cardinal pathological lesion of Alzheimer's disease (AD) is the deposition of amyloid beta (Abeta) in the brain. We previously reported that exposing transgenic mice harboring APPswe/PS1deltaE9 transgenes to an enriched environment resulted in reduced levels of Abeta 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 Abeta peptides and modulate their aggregation in vitro and in vivo. To explore the impact of TTR expression on Abeta levels and deposition in vivo, we crossed ceAPPswe/PS1deltaE9 transgenic mice to mice with genetic ablations of TTR. We now report that the levels of detergent-soluble and formic acid-soluble levels of Abeta and deposition are elevated in the brains of ceAPPswe/PS1deltaE9/TTR+/- mice compared with age-matched ceAPPswe/PS1deltaE9/TTR+/+ mice. Moreover, Abeta deposition is significantly accelerated in the hippocampus and cortex of ceAPPswe/PS1deltaE9/TTR+/- mice. Our results strongly suggest that TTR plays a critical role in modulating Abeta deposition in vivo.

Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin). Publishing Authors By Initials

SH Choi,SN Leight,VM Lee,T Li,PC Wong,JA Johnson,MJ Saraiva,SS Sisodia,

For similar genetic processes: gene expression regulation: up-regulation research abstracts see: genetic processes: gene expression regulation: up-regulation research

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Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin). Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of neuroscience : the official journal

VOLUME: 27

Page Numbers: 7006-10

Journal Abbreviation: J. Neurosci.

ISSN: 1529-2401

DAY: 27

MONTH: Jun

YEAR: 2007

Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin). Information

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LANGUAGE: eng

NlmUniqueID: 8102140

Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin). Keywords Mesh Terms:

KEYWORDS: Up-Regulation

MESH TERMS: genetics

Chemical & Substance for Abstract: Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin). Information

Substance Name: Presenilin-1

Registry Number: 0

Grant and Affiliation Information for Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin).

AFFILIATION: Committee on Neurobiology, University of Chicago, Chicago, Illinois 60637, USA.

Country: United States

AGENCY: United States NIA

GRANT: AG027854

ACRONYM: AG

MEDLINETA: J Neurosci

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