Low-n oligomers as therapeutic targets of Alzheimer's disease.
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.
Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan. onoken@med.kanazawa-u.ac.jp
Kenjiro
K
Ono
Masahito
M
Yamada
D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000737:chemistry* / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002478:Cells, Cultured; D019281:Dimerization; D004195:Disease Models, Animal; D016503:Drug Delivery Systems / Q000379:methods*; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D010446:Peptide Fragments / Q000737:chemistry* / Q000235:genetics / Q000378:metabolism*
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments