Transverse relaxation time reflects brain amyloidosis in young APP/PS1 transgenic mice

被引:27
|
作者
El Tayara, Nadine El Tannir
Volk, Andreas
Dhenain, Marc
Delatour, Benoit
机构
[1] CEA, URA 2210, CNRS, SHFJ, F-91401 Orsay, France
[2] Ctr Univ Orsay, INSERM U759, F-91405 Orsay, France
[3] Ctr Univ Orsay, Inst Curie, Res Ctr, F-91405 Orsay, France
[4] Univ Paris 11, UMR 8620, CNRS, Lab NAMC, Orsay, France
关键词
Alzheimer's disease; amyloid-beta peptide; iron; T-2; transgenic mouse;
D O I
10.1002/mrm.21266
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
Amyloid deposits are one of the hallmarks of Alzheimer's disease (AD), one of the most devastating neurodegenerative disorders. In transgenic mice modeling Alzheimer's pathology, the MR transverse relaxation time (T-2) has been described to be modulated by amyloidosis. This modification has been attributed to the age-related iron deposition that occurs within the amyloid plaques of old animals. In the present study, young APP/PS1 transgenic mice without histochemically detectable iron in the brain were specifically studied. In vivo measurements of T-2 in the hippocampus, at the level of the subiculum, were shown to reflect the density of amyloid plaques. This suggests that T-2 variations can be induced solely by aggregated amyloid deposits in the absence of associated histologically-detectable iron. Thus T-2 from regions with high amyloid load, such as the subiculum, is particularly well suited for following plaque deposition in young animals, i.e., at the earliest stages of the pathological process. Magn Reson Med 58:179-184, 2007. (c) 2007 Wiley-Liss, Inc.
引用
收藏
页码:179 / 184
页数:6
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