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β-Amyloid Is Different in Normal Aging and in Alzheimer Disease

2005; Elsevier BV; Volume: 280; Issue: 40 Linguagem: Inglês

10.1074/jbc.m501694200

1083-351X

Alessandra Piccini, Claudio Russo, Alessandra Gliozzi, Annalisa Relini, Antonella Vitali, Roberta Borghi, Luca Giliberto, Andrea Armirotti, Cristina D’Arrigo, Angela Bachi, Angela Cattaneo, Claudio Canale, Silvia Torrassa, Takaomi C. Saido, William R. Markesbery, Pierluigi Gambetti, Massimo Tabaton,

Neurological Disorders and Treatments

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.