A transgenic rat expressing human APP with the Swedish Alzheimer's disease mutation

被引:35
作者
Folkesson, Ronnie
Malkiewicz, Katarzyna
Kloskowska, Ewa
Nilsson, Tatjana
Popova, Elena
Bogdanovic, Nenad
Ganten, Ursula
Ganten, Detlev
Bader, Michael
Winblad, Bengt
Benedikz, Eirikur
机构
[1] Karolinska Inst, Dept Neurobiol Caring Sci & Soc, Div Neurodegenerat & Neuroinflammat, S-14186 Stockholm, Sweden
[2] Karolinska Inst, Dept Neurobiol Caring Sci & Soc, S-14186 Stockholm, Sweden
[3] Max Delbruck Ctr Mol Med, Berlin, Germany
关键词
Alzheimer's disease; amyloid precursor protein; transgenic; rat; amyloid; tau;
D O I
10.1016/j.bbrc.2007.04.195
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
In recent years, transgenic mice have become valuable tools for studying mechanisms of Alzheimer's disease (AD). With the aim of developing an animal model better for memory and neurobehavioural testing, we have generated a transgenic rat model of AD. These animals express human amyloid precursor protein (APP) containing the Swedish AD mutation. The highest level of expression in the brain is found in the cortex, hippocampus, and cerebellum. Starting after the age of 15 months, the rats show increased tau phosphorylation and extracellular A staining. The AP is found predominantly in cerebrovascular blood vessels with very rare diffuse plaques. We believe that crossing these animals with mutant PSI transgenic rats will result in accelerated plaque formation similar to that seen in transgenic mice. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:777 / 782
页数:6
相关论文
共 22 条
[1]
Animal models of neurological deficits: how relevant is the rat? [J].
Cenci, MA ;
Whishaw, IQ ;
Schallert, T .
NATURE REVIEWS NEUROSCIENCE, 2002, 3 (07) :574-579
[2]
IDENTIFICATION, TRANSMEMBRANE ORIENTATION AND BIOGENESIS OF THE AMYLOID A4 PRECURSOR OF ALZHEIMERS-DISEASE [J].
DYRKS, T ;
WEIDEMANN, A ;
MULTHAUP, G ;
SALBAUM, JM ;
LEMAIRE, HG ;
KANG, J ;
MULLERHILL, B ;
MASTERS, CL ;
BEYREUTHER, K .
EMBO JOURNAL, 1988, 7 (04) :949-957
[3]
Altered mitogen-activated protein kinase signaling, tau hyperphosphorylation and mild spatial learning dysfunction in transgenic rats expressing the β-amyloid peptide intracellularly in hippocampal and cortical neurons [J].
Echeverria, V ;
Ducatenzeiler, A ;
Dowd, E ;
Jänne, E ;
Grant, SM ;
Szyf, M ;
Wandosell, F ;
Avila, J ;
Grimm, H ;
Dunnett, SB ;
Hartmann, T ;
Alhonen, L ;
Cuello, AC .
NEUROSCIENCE, 2004, 129 (03) :583-592
[4]
Echeverria V, 2004, J ALZHEIMERS DIS, V6, P209
[5]
Alzheimer transgenic models [J].
Folkesson, R ;
Winblad, B ;
Benedikz, E .
CURRENT OPINION IN PSYCHIATRY, 2002, 15 (04) :433-439
[6]
Transgenic mouse models of Alzheimer's disease: phenotype and application [J].
Higgins, GA ;
Jacobsen, H .
BEHAVIOURAL PHARMACOLOGY, 2003, 14 (5-6) :419-438
[7]
Behavioral phenotypes of amyloid-based genetically modified mouse models of Alzheimer's disease [J].
Kobayashi, DT ;
Chen, KS .
GENES BRAIN AND BEHAVIOR, 2005, 4 (03) :173-196
[8]
The evolution of Aβ peptide burden in the APP23 transgenic mice:: Implications for Aβ deposition in Alzheimer disease [J].
Kuo, YM ;
Beach, TG ;
Sue, LI ;
Scott, S ;
Layne, KJ ;
Kokjohn, TA ;
Kalback, WM ;
Luehrs, DC ;
Vishnivetskaya, TA ;
Abramowski, D ;
Sturchler-Pierrat, C ;
Staufenbiel, M ;
Weller, RO ;
Roher, AE .
MOLECULAR MEDICINE, 2001, 7 (09) :609-618
[9]
Lopez EM, 2004, J ALZHEIMERS DIS, V6, P421
[10]
Improved survival of embryonic porcine dopaminergic neurons in coculture with a conditionally immortalized GDNF-producing hippocampal cell line [J].
Meyer, M ;
Johansen, J ;
Gramsbergen, JB ;
Johansen, TE ;
Zimmer, J .
EXPERIMENTAL NEUROLOGY, 2000, 164 (01) :82-93