Amyloid β

被引：30

作者：

Cappai, R ^{[1
]}

White, AR

机构：

[1] Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia

[2] Mental Hlth Res Inst, Parkville, Vic 3052, Australia

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 1999年 / 31卷 / 09期

关键词：

Alzheimer's disease; neurotoxicity; neurodegeneration; amyloid precursor protein;

D O I：

10.1016/S1357-2725(99)00027-8

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：

Amyloid beta (A beta) is a 39-43 residue amyloidogenic peptide that is deposited into the extracellular amyloid plaques which characterize an Alzheimer's disease (AD) brain. A beta is derived from the amyloid precursor protein (APP) and undergoes a toxic conformational change (gain of toxic function). The length of the A beta peptide dramatically influences its properties with the longer 42 and 43 residue species being more amyloidogenic. The genetics of familial AD (FAD) supports a central role for A beta in AD since mutations in the FAD causing genes APP and the presenilins (PS1 and PS2) increase the formation of A beta 42,43, Considerable activity is directed towards A beta as a therapeutic target. These strategies aim to inhibit A beta synthesis, A beta fibril formation, its toxic actions on cells or promote its clearance from the brain. (C) 1999 Elsevier Science Ltd. All rights reserved.

引用

页码：885 / 889

页数：5

共 19 条

[1] Dramatic aggregation of Alzheimer Aβ by Cu(II) is induced by conditions representing physiological acidosis [J].

Atwood, CS ;

Moir, RD ;

Huang, XD ;

Scarpa, RC ;

Bacarra, NME ;

Romano, DM ;

Hartshorn, MK ;

Tanzi, RE ;

Bush, AI .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (21) :12817-12826

[2]

Blanc EM, 1997, J NEUROCHEM, V68, P1870

[3] Promotion of transition metal-induced reactive oxygen species formation by β-amyloid [J].

Bondy, SC ;

Guo-Ross, SX ;

Truong, AT .

BRAIN RESEARCH, 1998, 799 (01) :91-96

[4] The SREBP pathway: Regulation of cholesterol metabolism by proteolysis of a membrane-bound transcription factor [J].

Brown, MS ;

Goldstein, JL .

CELL, 1997, 89 (03) :331-340

[5] Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein [J].

De Strooper, B ;

Saftig, P ;

Craessaerts, K ;

Vanderstichele, H ;

Guhde, G ;

Annaert, W ;

Von Figura, K ;

Van Leuven, F .

NATURE, 1998, 391 (6665) :387-390

[6] Recent work on Alzheimer's disease transgenics [J].

Duff, K .

CURRENT OPINION IN BIOTECHNOLOGY, 1998, 9 (06) :561-564

[7] ALZHEIMERS-DISEASE AND DOWNS-SYNDROME - SHARING OF A UNIQUE CEREBROVASCULAR AMYLOID FIBRIL PROTEIN [J].

GLENNER, GG ;

WONG, CW .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1984, 122 (03) :1131-1135

[8] Amyloid, the presenilins and Alzheimer's disease [J].

Hardy, J .

TRENDS IN NEUROSCIENCES, 1997, 20 (04) :154-159

[9] β-amyloid induces local neurite degeneration in cultured hippocampal neurons:: Evidence for neuritic apoptosis [J].

Ivins, KJ ;

Bui, ETN ;

Cotman, CW .

NEUROBIOLOGY OF DISEASE, 1998, 5 (05) :365-378

[10] SEEDING ONE-DIMENSIONAL CRYSTALLIZATION OF AMYLOID - A PATHOGENIC MECHANISM IN ALZHEIMERS-DISEASE AND SCRAPIE [J].

JARRETT, JT ;

LANSBURY, PT .

CELL, 1993, 73 (06) :1055-1058

← 1 2 →