Low-n oligomers as therapeutic targets of Alzheimer’s disease
Article first published online: 9 FEB 2011
© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry
Journal of Neurochemistry
Volume 117, Issue 1, pages 19–28, April 2011
How to Cite
Ono, K. and Yamada, M. (2011), Low-n oligomers as therapeutic targets of Alzheimer’s disease. Journal of Neurochemistry, 117: 19–28. doi: 10.1111/j.1471-4159.2011.07187.x
- Issue published online: 11 MAR 2011
- Article first published online: 9 FEB 2011
- Accepted manuscript online: 18 JAN 2011 03:17PM EST
- Received December 6, 2010; revised manuscript received January 10, 2011; accepted January 12, 2011.
- Alzheimer’s disease;
- amyloid β-protein;
J. Neurochem. (2011) 117, 19–28.
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.