Low-n oligomers as therapeutic targets of Alzheimer’s disease

Authors


Address correspondence and reprint requests to Dr K. Ono, Department of Neurology & Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8640, Japan. E-mail: onoken@med.kanazawa-u.ac.jp

Abstract

J. Neurochem. (2011) 117, 19–28.

Abstract

The pathogenesis of Alzheimer’s disease involves the progressive accumulation of amyloid β-protein (Aβ). Recent studies using synthetic Aβ peptides, a cell culture model, Aβ precursor protein transgenic mice models suggest that pre-fibrillar forms of Aβ are more deleterious than extracellular fibril forms. Recent findings obtained using synthetic Aβ peptides and human samples indicated that low-n oligomers (from dimers to octamers) may be proximate toxins for neuron and synapse. Here, we review the recent studies on the soluble oligomers, especially low-n oligomers in Alzheimer’s disease.

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