The role of intracellular amyloid β in Alzheimer's disease

被引：111

作者：

Li, Meng

Chen, Liying

Lee, Daniel Hong Seng

Yu, Long-Chuan

Zhang, Yan

机构：

[1] Peking Univ, Coll Life Sci, Lab Neurobiol, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China

[2] Biogen Inc, Cambridge, MA 02142 USA

来源：

PROGRESS IN NEUROBIOLOGY | 2007年 / 83卷 / 03期

基金：

中国国家自然科学基金;

关键词：

Alzheimer's disease; amyloid p peptide; neurotoxicity; neuronal loss;

D O I：

10.1016/j.pneurobio.2007.08.002

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Extracellular amyloid beta (A beta) that confers neurotoxicity and modulates synaptic plasticity and memory function has been central to the amyloid hypothesis of Alzheimer's disease (AD) pathology. Like many other misfolded proteins identified in neurodegenerative disorders, A beta also accumulates inside the AD neurons. This intracellular A beta affects a variety of cellular physiology from protein degradation, axonal transport, autophagy to apoptosis, further documenting the role of A beta in AD. Therapeutics targeting intracellular A beta could be effective treatment for AD. (c) 2007 Elsevier Ltd. All rights reserved.

引用

页码：131 / 139

页数：9

共 134 条

[1] Caspase 6 activity initiates caspase 3 activation in cerebellar granule cell apoptosis [J].

Allsopp, TE ;

McLuckie, J ;

Kerr, LE ;

Macleod, M ;

Sharkey, J ;

Kelly, JS .

CELL DEATH AND DIFFERENTIATION, 2000, 7 (10) :984-993

[2] β-amyloid accumulation impairs multivesicular body sorting by inhibiting the ubiquitin-proteasome system [J].

Almeida, CG ;

Takahashi, RH ;

Gouras, GK .

JOURNAL OF NEUROSCIENCE, 2006, 26 (16) :4277-4288

[3]

ASKANAS V, 1992, AM J PATHOL, V141, P31

[4] Molecular imaging with Pittsburgh compound B confirmed at autopsy - A case report [J].

Bacskai, Brian J. ;

Frosch, Matthew P. ;

Freeman, Stefanie H. ;

Raymond, Scott B. ;

Augustinack, Jean C. ;

Johnson, Keith A. ;

Irizarry, Michael C. ;

Klunk, William E. ;

Mathis, Chester A. ;

DeKosky, Steven T. ;

Greenberg, Steven M. ;

Hyman, Bradley T. ;

Growdon, John H. .

ARCHIVES OF NEUROLOGY, 2007, 64 (03) :431-434

[5] The neuropathogenic contributions of lysosomal dysfunction [J].

Bahr, BA ;

Bendiske, J .

JOURNAL OF NEUROCHEMISTRY, 2002, 83 (03) :481-489

[6] HYDROGEN-PEROXIDE MEDIATES AMYLOID-BETA PROTEIN TOXICITY [J].

BEHL, C ;

DAVIS, JB ;

LESLEY, R ;

SCHUBERT, D .

CELL, 1994, 77 (06) :817-827

[7] Lysosomal activation is a compensatory response against protein accumulation and associated synaptopathogenesis - An approach for slowing Alzheimer disease? [J].

Bendiske, J ;

Bahr, BA .

JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2003, 62 (05) :451-463

[8] Intraneuronal Aβ causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice [J].

Billings, LM ;

Oddo, S ;

Green, KN ;

McGaugh, JL ;

LaFerla, FM .

NEURON, 2005, 45 (05) :675-688

[9] Cell death in the nervous system [J].

Bredesen, Dale E. ;

Rao, Rammohan V. ;

Mehlen, Patrick .

NATURE, 2006, 443 (7113) :796-802

[10] Altered metabolism of the amyloid β precursor protein is associated with mitochondrial dysfunction in Down's syndrome [J].

Busciglio, J ;

Pelsman, A ;

Wong, C ;

Pigino, G ;

Yuan, ML ;

Mori, H ;

Yankner, BA .

NEURON, 2002, 33 (05) :677-688

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