Amyloid β-Protein Assembly and Alzheimer Disease

被引：517

作者：

Roychaudhuri, Robin ^{[1
]}

Yang, Mingfeng ^{[1
]}

Hoshi, Minako M. ^{[2
]}

Teplow, David B. ^{[1
]}

机构：

[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA

[2] Mitsubishi Kagaku Inst Life Sci, Tokyo 1948511, Japan

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2009年 / 284卷 / 08期

关键词：

OXIDATIVE STRESS; MITOCHONDRIAL DYSFUNCTION; PEPTIDE; NEURODEGENERATION; AGGREGATION; NEUROTOXICITY; MECHANISMS; MEMBRANE; DISTINCT; FIBRILS;

D O I：

10.1074/jbc.R800036200

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：

引用

页码：4749 / 4753

页数：5

共 50 条

[31] On the nucleation and growth of amyloid beta-protein fibrils: Detection of nuclei and quantitation of rate constants [J].

Lomakin, A ;

Chung, DS ;

Benedek, GB ;

Kirschner, DA ;

Teplow, DB .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (03) :1125-1129

[32] Soluble oligomers of amyloid-β peptide induce neuronal apoptosis by activating a cPLA2-dependent sphingomyelinase-ceramide pathway [J].

Malaplate-Armand, Catherine ;

Florent-Bechard, Sabrina ;

Youssef, Ihsen ;

Koziel, Violette ;

Sponne, Isabelle ;

Kriem, Badreddine ;

Leininger-Muller, Brigitte ;

Olivier, Jean-Luc ;

Oster, Thierry ;

Pillot, Thierry .

NEUROBIOLOGY OF DISEASE, 2006, 23 (01) :178-189

[33] Mitochondrial dysfunction, free radical generation and cellular stress response in neurodegenerative disorders [J].

Mancuso, Cesare ;

Scapagnini, Giovanni ;

Curro, Diego ;

Giuffrida Stella, Anna Maria ;

De Marco, Carlo ;

Butterfield, D. Allan ;

Calabrese, Vittorio .

FRONTIERS IN BIOSCIENCE-LANDMARK, 2007, 12 :1107-1123

[34] Formation and stabilization model of the 42-mer Aβ radical:: Implications for the long-lasting oxidative stress in Alzheimer's disease [J].

Murakami, K ;

Irie, K ;

Ohigashi, H ;

Hara, H ;

Nagao, M ;

Shimizu, T ;

Shirasawa, T .

JOURNAL OF THE AMERICAN CHEMICAL SOCIETY, 2005, 127 (43) :15168-15174

[35] Small molecule inhibitors of aggregation indicate that amyloid β oligomerization and fibrillization pathways are independent and distinct [J].

Necula, Mihaela ;

Kayed, Rakez ;

Milton, Saskia ;

Glabe, Charles G. .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2007, 282 (14) :10311-10324

[36] Recent atomic models of amyloid fibril structure [J].

Nelson, R ;

Eisenberg, D .

CURRENT OPINION IN STRUCTURAL BIOLOGY, 2006, 16 (02) :260-265

[37] Atomic structures of amyloid cross-β spines reveal varied steric zippers [J].

Sawaya, Michael R. ;

Sambashivan, Shilpa ;

Nelson, Rebecca ;

Ivanova, Magdalena I. ;

Sievers, Stuart A. ;

Apostol, Marcin I. ;

Thompson, Michael J. ;

Balbirnie, Melinda ;

Wiltzius, Jed J. W. ;

McFarlane, Heather T. ;

Madsen, Anders O. ;

Riekel, Christian ;

Eisenberg, David .

NATURE, 2007, 447 (7143) :453-457

[38]

Sipe JD, 2005, AMYLOID PROTEINS: THE BETA SHEET CONFORMATION AND DISEASE, VOLS 1 AND 2, P1, DOI 10.1002/9783527619344

[39]

Sokolov Yuri, 2006, J Gen Physiol, V128, P637, DOI 10.1085/jgp.200609533

[40] The effect of cholesterol and monosialoganglioside (GM1) on the release and aggregation of amyloid β-peptide from liposomes prepared from brain membrane-like lipids [J].

Tashima, Y ;

Oe, R ;

Lee, S ;

Sugihara, G ;

Chambers, EJ ;

Takahashi, M ;

Yamada, T .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (17) :17587-17595

← 1 2 3 4 5 →