Mechanisms of memory loss in Aβ and tau mouse models

被引:31
作者
Ashe, KH [1 ]
机构
[1] Univ Minnesota, Dept Neurol, Minneapolis, MN 55455 USA
[2] Univ Minnesota, Dept Neurosci, Minneapolis, MN 55455 USA
[3] Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Minneapolis, MN 55417 USA
关键词
A beta; Alzheimer's disease; amyloid plaque; APP transgenic mice; memory loss; tau;
D O I
10.1042/BST0330591
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Although memory loss is the central symptom of Alzheimer's disease, the pathophysiological mechanisms leading to dementia are poorly understood. it is difficult to answer this issue with studies in humans and impossible in cultured cells. Therefore animal models are needed to elucidate the molecular mechanisms leading to dementia. The chief neuropathological changes during Alzheimer's disease, namely neurofibrillary tangles and amyloid plaques, have helped us to determine which molecules to focus upon in the animal models, specifically A beta (amyloid beta) and tau. This paper presents my perspective on what we have learnt about mechanisms of memory loss from A beta and tau mouse models of Alzheimer's disease.
引用
收藏
页码:591 / 594
页数:4
相关论文
共 54 条
[1]   Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms [J].
Andorfer, C ;
Kress, Y ;
Espinoza, M ;
de Silva, R ;
Tucker, KL ;
Barde, YA ;
Duff, K ;
Davies, P .
JOURNAL OF NEUROCHEMISTRY, 2003, 86 (03) :582-590
[2]   Learning and memory in Transgenic mice Modeling Alzheimer's disease [J].
Ashe, KH .
LEARNING & MEMORY, 2001, 8 (06) :301-308
[3]   Evidence for glial-mediated inflammation in aged APPSW transgenic mice [J].
Benzing, WC ;
Wujek, JR ;
Ward, EK ;
Shaffer, D ;
Ashe, KH ;
Younkin, SG ;
Brunden, KR .
NEUROBIOLOGY OF AGING, 1999, 20 (06) :581-589
[4]   Patterns of brain activation in people at risk for Alzheimer's disease [J].
Bookheimer, SY ;
Strojwas, MH ;
Cohen, MS ;
Saunders, AM ;
Pericak-Vance, MA ;
Mazziotta, JC ;
Small, GW .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (07) :450-456
[5]   Neuron loss in APP transgenic mice [J].
Calhoun, ME ;
Wiederhold, KH ;
Abramowski, D ;
Phinney, AL ;
Probst, A ;
Sturchler-Pierrat, C ;
Staufenbiel, M ;
Sommer, B ;
Jucker, M .
NATURE, 1998, 395 (6704) :755-756
[6]   Natural oligomers of the amyloid-protein specifically disrupt cognitive function [J].
Cleary, JP ;
Walsh, DM ;
Hofmeister, JJ ;
Shankar, GM ;
Kuskowski, MA ;
Selkoe, DJ ;
Ashe, KH .
NATURE NEUROSCIENCE, 2005, 8 (01) :79-84
[7]   Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model [J].
Dodart, JC ;
Bales, KR ;
Gannon, KS ;
Greene, SJ ;
DeMattos, RB ;
Mathis, C ;
DeLong, CA ;
Wu, S ;
Wu, X ;
Holtzman, DM ;
Paul, SM .
NATURE NEUROSCIENCE, 2002, 5 (05) :452-457
[8]   Neuropathology and pathogenesis of encephalitis following amyloid-β immunization in Alzheimer's disease [J].
Ferrer, I ;
Rovira, MB ;
Guerra, MLS ;
Rey, MJ ;
Costa-Jussá, F .
BRAIN PATHOLOGY, 2004, 14 (01) :11-20
[9]  
Frautschy SA, 1998, AM J PATHOL, V152, P307
[10]   ALZHEIMER-TYPE NEUROPATHOLOGY IN TRANSGENIC MICE OVEREXPRESSING V717F BETA-AMYLOID PRECURSOR PROTEIN [J].
GAMES, D ;
ADAMS, D ;
ALESSANDRINI, R ;
BARBOUR, R ;
BERTHELETTE, P ;
BLACKWELL, C ;
CARR, T ;
CLEMENS, J ;
DONALDSON, T ;
GILLESPIE, F ;
GUIDO, T ;
HAGOPIAN, S ;
JOHNSONWOOD, K ;
KHAN, K ;
LEE, M ;
LEIBOWITZ, P ;
LIEBERBURG, I ;
LITTLE, S ;
MASLIAH, E ;
MCCONLOGUE, L ;
MONTOYAZAVALA, M ;
MUCKE, L ;
PAGANINI, L ;
PENNIMAN, E ;
POWER, M ;
SCHENK, D ;
SEUBERT, P ;
SNYDER, B ;
SORIANO, F ;
TAN, H ;
VITALE, J ;
WADSWORTH, S ;
WOLOZIN, B ;
ZHAO, J .
NATURE, 1995, 373 (6514) :523-527