In vitro models of age-related neurodegenerative disorders

被引：8

作者：

Delacourte, A ^{[1
]}

Sergeant, N ^{[1
]}

Buée, L ^{[1
]}

机构：

[1] INSERM, U422, Inst Med Predict & Rech Therapeut, F-59045 Lille, France

来源：

EXPERIMENTAL GERONTOLOGY | 2003年 / 38卷 / 11-12期

关键词：

alzheimer's disease; neurodegenerative disorder; aging;

D O I：

10.1016/j.exger.2003.09.010

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：

Aging is the major risk factor for numerous brain diseases. This is especially true for Alzheimer's disease (AD), a peculiar neurodegenerative disorder in that it results from the synergy of two simultaneous but distinct degenerating processes: Abeta and tau pathologies. For AD, and for most neurodegenerative disorders, aggregation of full length or truncated proteins, in neurons or glial cells, or in the parenchyma, is central, but still a mystery. In addition, the late onset of these pathologies links them to ageing processes. Cause or consequence? Experimental models, that allow us to dissect these pathophysiological defects, are presented. (C) 2003 Elsevier Inc. All rights reserved.

引用

页码：1309 / 1317

页数：9

共 60 条

[41] AMINO-TERMINAL DELETIONS ENHANCE AGGREGATION OF BETA-AMYLOID PEPTIDES IN-VITRO
PIKE, CJ
OVERMAN, MJ
COTMAN, CW
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (41) : 23895 - 23898
[42] Inhibition of protein phosphatase 2A overrides tau protein kinase I/glycogen synthase kinase 3β and cyclin-dependent kinase 5 inhibition and results in tau hyperphosphorylation in the hippocampus of starved mouse
Planel, E
Yasutake, K
Fujita, SC
Ishiguro, K
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (36) : 34298 - 34306
[43] Mutation in the alpha-synuclein gene identified in families with Parkinson's disease
Polymeropoulos, MH
Lavedan, C
Leroy, E
Ide, SE
Dehejia, A
Dutra, A
Pike, B
Root, H
Rubenstein, J
Boyer, R
Stenroos, ES
Chandrasekharappa, S
Athanassiadou, A
Papapetropoulos, T
Johnson, WG
Lazzarini, AM
Duvoisin, RC
DiIorio, G
Golbe, LI
Nussbaum, RL
[J]. SCIENCE, 1997, 276 (5321) : 2045 - 2047
[44] Pyroglutamate-modified amyloid β-peptides -: AβN3(pE)-strongly affect cultured neuron and astrocyte survival
Russo, C
Violani, E
Salis, S
Venezia, V
Dolcini, V
Damonte, G
Benatti, U
D'Arrigo, C
Patrone, E
Carlo, P
Schettini, G
[J]. JOURNAL OF NEUROCHEMISTRY, 2002, 82 (06) : 1480 - 1489
[45] Schultz C, 2001, ADV EXP MED BIOL, V487, P59
[46] Truncated beta-amyloid peptide species in pre-clinical Alzheimer's disease as new targets for the vaccination approach
Sergeant, N
Bombois, S
Ghestem, A
Drobecq, H
Kostanjevecki, V
Missiaen, C
Wattez, A
David, JP
Vanmechelen, E
Sergheraert, C
Delacourte, A
[J]. JOURNAL OF NEUROCHEMISTRY, 2003, 85 (06) : 1581 - 1591
[47] Sergeant N, 1997, J NEUROCHEM, V69, P834
[48] Progressive decrease of amyloid precursor protein carboxy terminal fragments (APP-CTFs), associated with tau pathology stages, in Alzheimer's disease
Sergeant, N
David, JP
Champain, D
Ghestem, A
Wattez, A
Delacourte, A
[J]. JOURNAL OF NEUROCHEMISTRY, 2002, 81 (04) : 663 - 672
[49] Fiber diffraction of synthetic α-synuclein filaments shows amyloid-like cross-β conformation
Serpell, LC
Berriman, J
Jakes, R
Goedert, M
Crowther, RA
[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (09) : 4897 - 4902
[50] Generation of amyloid β peptide with pyroglutamate at position 3 in primary cortical neurons
Shirotani, K
Tsubuki, S
Lee, HJ
Maruyama, K
Saido, TC
[J]. NEUROSCIENCE LETTERS, 2002, 327 (01) : 25 - 28

← 1 2 3 4 5 6 →