Early onset amyloid lesions lead to severe neuritic abnormalities and local, but not global neuron loss in APPPS1 transgenic mice

被引：65

作者：

Rupp, Niels J. ^{[1
,2
]}

Wegenast-Braun, Bettina M. ^{[1
,2
]}

Radde, Rebecca ^{[1
]}

Calhoun, Michael E. ^{[1
,3
]}

Jucker, Mathias ^{[1
,2
]}

机构：

[1] Univ Tubingen, Dept Cellular Neurol, Hertie Inst Clin Brain Res, D-72076 Tubingen, Germany

[2] DZNE German Ctr Neurodegenerat Dis, Tubingen, Germany

[3] Sinq Syst, Columbia, MD USA

来源：

NEUROBIOLOGY OF AGING | 2011年 / 32卷 / 12期

关键词：

Alzheimer's disease; Neocortex; Hippocampus; Stereology; ALZHEIMERS-DISEASE; BETA DEPOSITION; SELECTIVE LOSS; MOUSE MODELS; PRESENILIN-1; MUTATIONS; PATHOLOGY; DEMENTIA; PLAQUES; LAYER;

D O I：

10.1016/j.neurobiolaging.2010.08.014

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

APPPS1 transgenic mice develop amyloid-beta 42 (A beta 42)-driven early-onset cerebral beta-amyloidosis. Stereological analysis of neocortical neuron number in groups of 2-, 10-, and 17-month-old APPPS1 mice did not reveal any changes compared with wild-type control animals despite massive amyloid-beta (A beta) load and disrupted cytoarchitecture. However, in subregions with high neuron density such as the granule cell layer of the dentate gyrus, modest but significant neuron loss was found, reminiscent of findings in previously published mouse models with late onset cerebral beta-amyloidosis and predominant amyloid-beta 40 (A beta 40) expression. (C) 2011 Elsevier Inc. All rights reserved.

引用

页码：2324.e1 / 2324.e6

页数：6

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