β-amyloid is different in normal aging and in Alzheimer disease

被引：169

作者：

Piccini, A

Russo, C

Gliozzi, A

Relini, A

Vitali, A

Borghi, R

Giliberto, L

Armirotti, A

D'Arrigo, C

Bachi, A

Cattaneo, A

Canale, C

Torrassa, S

Saido, TC

Markesbery, W

Gambetti, P

Tabaton, M

机构：

[1] Univ Genoa, Dept Neurosci Ophthalmol & Genet, I-16132 Genoa, Italy

[2] Univ Genoa, Dept Oncol Biol & Genet, I-16132 Genoa, Italy

[3] Univ Genoa, Dept Phys, I-16132 Genoa, Italy

[4] Univ Genoa, Ctr Excellence Biomed Res, Dept Expt Med, I-16132 Genoa, Italy

[5] CNR, Inst Macromol Res, I-16149 Genoa, Italy

[6] San Raffaele Fdn, Dept Biotechnol, I-20132 Milan, Italy

[7] RIKEN Brain Sci Inst, Saitama 3510198, Japan

[8] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40536 USA

[9] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2005年 / 280卷 / 40期

关键词：

D O I：

10.1074/jbc.M501694200

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：

The mechanism of neurodegeneration caused by beta-amyloid in Alzheimer disease is controversial. Neuronal toxicity is exerted mostly by various species of soluble beta-amyloid oligomers that differ in their N- and C-terminal domains. However, abundant accumulation of beta-amyloid also occurs in the brains of cognitively normal elderly people, in the absence of obvious neuronal dysfunction. We postulated that neuronal toxicity depends on the molecular composition, rather than the amount, of the soluble beta-amyloid oligomers. Here we show that soluble beta-amyloid aggregates that accumulate in Alzheimer disease are different from those of normal aging in regard to the composition as well as the aggregation and toxicity properties.

引用

页码：34186 / 34192

页数：7

共 37 条

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