J. Lipid Res.
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A more recent version of this article appeared on April 1, 2007

Papers In Press, published online ahead of print January 18, 2007
J. Lipid Res., doi:10.1194/jlr.M600543-JLR200
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Submitted on December 21, 2006
Accepted on January 17, 2007

Physiologically regulated transgenic ABCA1 does not reduce amyloid burden or Abeta levels in vivo

Veronica Hirsch-Reinshagen, Jennifer Y. Chan, Anna Wilkinson, Tracie Tanaka, Jianjia Fan, George Ou, Luis F. Maia, Roshni R. Singaraja, Michael R. Hayden, and Cheryl L. Wellington

Pathology Dept., University of British Columbia, Vancouver, BC V5Z 4H4

Corresponding Author: cheryl{at}cmmt.ubc.ca

ABCA1-deficient mice have low levels of poorly-lipidated apoE and exhibit increased amyloid load. To test whether excess ABCA1 protects from amyloid deposition, we crossed APP/PS1 mice to ABCA1 bacterial artificial chromosome (BAC) transgenic mice. Compared to wild-type animals, the ABCA1 BAC led to a 50% increase in cortical ABCA1 protein and a 15% increase in apoE abundance, demonstrating that this BAC supports modest ABCA1 overexpression in brain. However, this was only observed in animals that do not deposit amyloid. Comparison of ABCA1/APP/PS1 mice with APP/PS1 controls revealed no differences in levels of brain ABCA1 protein, amyloid, Abeta , or apoE, despite clear retention of ABCA1 overexpression in the livers of these animals. To further investigate ABCA1 expression in the amyloid-containing brain, we then compared ABCA1 mRNA and protein levels in young and aged cortex and cerebellum of APP/PS1 and ABCA1/APP/PS1 animals. Compared to APP/PS1 controls, aged ABCA1/APP/PS1 mice exhibited elevated ABCA1 mRNA but not protein, selectively in cortex. Additionally, ABCA1 mRNA levels are not elevated prior to amyloid deposition, but are induced only in the presence of extensive Abeta and amyloid levels. These data suggest that an induction of ABCA1 expression may be associated with late-stage Alzheimer’s neuropathology.


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B. L. Burgess, P. F. Parkinson, M. M. Racke, V. Hirsch-Reinshagen, J. Fan, C. Wong, S. Stukas, L. Theroux, J. Y. Chan, J. Donkin, et al.
ABCG1 influences the brain cholesterol biosynthetic pathway but does not affect amyloid precursor protein or apolipoprotein E metabolism in vivo
J. Lipid Res., June 1, 2008; 49(6): 1254 - 1267.
[Abstract] [Full Text] [PDF]


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