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

摘要: J. Neurochem. (2011) 117, 19–28. Abstract The pathogenesis of Alzheimer’s disease involves the progressive accumulation amyloid β-protein (Aβ). Recent studies using synthetic Aβ peptides, a cell culture model, precursor protein transgenic mice models suggest that pre-fibrillar forms are more deleterious than extracellular fibril forms. findings obtained peptides and human samples indicated low-n oligomers (from dimers to octamers) may be proximate toxins for neuron synapse. Here, we review recent on soluble oligomers, especially in disease.