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Low‐n oligomers as therapeutic targets of Alzheimer’s disease
Author(s) -
Ono Kenjiro,
Yamada Masahito
Publication year - 2011
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2011.07187.x
Subject(s) - pathogenesis , extracellular , fibril , alzheimer's disease , genetically modified mouse , disease , amyloid (mycology) , synapse , neuroscience , chemistry , transgene , amyloid β , biochemistry , microbiology and biotechnology , biology , medicine , gene , immunology , pathology , inorganic chemistry
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.