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The folding of amyloid β-protein (Aβ) into oligomeric, protofibrillar, and fibrillar assemblies is hypothesized to be the key pathogenic event in Alzheimer's disease (AD), with oligomeric assemblies thought to be the most neurotoxic. Inhibitors of oligomer formation, therefore, could be valuable therapeutics for patients with AD. Epidemiological studies have indicated that estrogen therapy reduces...
Amyloid β-protein (Aβ) fibril in senile plaques may possibly be related to the pathogenesis of Alzheimer's disease (AD). Basement membrane (BM) components are localized to the plaques. Entactin binds the plaque associated BM components. We investigated the potential of entactin to prevent Aβ fibril formation. Thioflavin T fluorometric assay and electron microscopy revealed that entactin significantly...
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