Animal models of Alzheimer's disease and evaluation of anti-dementia drugs

被引：156

作者：

Yamada, K

Nabeshima, T ^{[1
]}

机构：

[1] Nagoya Univ, Grad Sch Med, Dept Neuropsychopharmacol, Showa Ku, Nagoya, Aichi 4668560, Japan

[2] Nagoya Univ, Hosp Pharm, Grad Sch Med, Showa Ku, Nagoya, Aichi 4668560, Japan

来源：

PHARMACOLOGY & THERAPEUTICS | 2000年 / 88卷 / 02期

关键词：

Alzheimer's disease; amyloid beta-peptide (A beta); beta-amyloid precursor protein (APP); tau; presenilins; animal model;

D O I：

10.1016/S0163-7258(00)00081-4

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Alzheimer's disease (AD) is the most common cause of progressive decline of cognitive function in aged humans, and is characterized by the presence of numerous senile plaques and neurofibrillary tangles accompanied by neuronal loss. Some, but not all, of the neuropathological alterations and cognitive impairment in AD can be reproduced genetically and pharmacologically in animals. It should be possible to discover novel drugs that slow the progress or alleviate the clinical symptoms of AD by using these animal models. We review the recent progress in the development of animal models of AD and discuss how to use these model animals to evaluate novel anti-dementia drugs. (C) 2000 Elsevier Science Inc. All rights reserved.

引用

收藏

页码：93 / 113

页数：21

相关论文

共 283 条

[1] Fibrillogenesis of β-amyloid [J].

Allsop, D ;

Howlett, D ;

Christie, G ;

Karran, E .

BIOCHEMICAL SOCIETY TRANSACTIONS, 1998, 26 (03) :459-463

[2]

Alvarez A, 1998, J NEUROSCI, V18, P3213

[3] Acetylcholinesterase promotes the aggregation of amyloid-beta-peptide fragments by forming a complex with the growing fibrils [J].

Alvarez, A ;

Opazo, C ;

Alarcon, R ;

Garrido, J ;

Inestrosa, NC .

JOURNAL OF MOLECULAR BIOLOGY, 1997, 272 (03) :348-361

[4] Reduced cerebrospinal fluid levels of α-secretase-cleaved amyloid precursor protein in aged rats:: Correlation with spatial memory deficits [J].

Anderson, JJ ;

Holtz, G ;

Baskin, PP ;

Wang, R ;

Mazzarelli, L ;

Wagner, SL ;

Menzaghi, F .

NEUROSCIENCE, 1999, 93 (04) :1409-1420

[5] EXACT CLEAVAGE SITE OF ALZHEIMER AMYLOID PRECURSOR IN NEURONAL PC-12 CELLS [J].

ANDERSON, JP ;

ESCH, FS ;

KEIM, PS ;

SAMBAMURTI, K ;

LIEBERBURG, I ;

ROBAKIS, NK .

NEUROSCIENCE LETTERS, 1991, 128 (01) :126-128

[6] PAIRED HELICAL FILAMENT-LIKE PHOSPHORYLATION OF TAU, DEPOSITION OF BETA/A4-AMYLOID AND MEMORY IMPAIRMENT IN RAT INDUCED BY CHRONIC INHIBITION OF PHOSPHATASE-1 AND PHOSPHATASE-2A [J].

ARENDT, T ;

HOLZER, M ;

FRUTH, R ;

BRUCKNER, MK ;

GARTNER, U .

NEUROSCIENCE, 1995, 69 (03) :691-698

[7] IN-VIVO PHOSPHORYLATION IN THE RAT BASAL NUCLEUS INDUCES PHF-LIKE AND APP IMMUNOREACTIVITY [J].

ARENDT, T ;

HANISCH, F ;

HOLZER, M ;

BRUCKNER, MK .

NEUROREPORT, 1994, 5 (11) :1397-1400

[8] NEUROFIBRILLARY TANGLES BUT NOT SENILE PLAQUES PARALLEL DURATION AND SEVERITY OF ALZHEIMERS-DISEASE [J].

ARRIAGADA, PV ;

GROWDON, JH ;

HEDLEYWHYTE, ET ;

HYMAN, BT .

NEUROLOGY, 1992, 42 (03) :631-639

[9] β-amyloid peptides as direct cholinergic neuromodulators:: a missing link? [J].

Auld, DS ;

Kar, S ;

Quirion, R .

TRENDS IN NEUROSCIENCES, 1998, 21 (01) :43-49

[10] Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition [J].

Bales, KR ;

Verina, T ;

Dodel, RC ;

Du, YS ;

Altstiel, L ;

Bender, M ;

Hyslop, P ;

Johnstone, EM ;

Little, SP ;

Cummins, DJ ;

Piccardo, P ;

Ghetti, B ;

Paul, SM .

NATURE GENETICS, 1997, 17 (03) :263-264

← 1 2 3 4 5 6 7 8 9 10 →