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Neurobiol Aging. 2010 Apr;31(4):542-8. doi: 10.1016/j.neurobiolaging.2008.05.026. Epub 2008 Jul 10.

Molecular polymorphism of Abeta in Alzheimer's disease.

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1
Department of Molecular and Cellular Biochemistry, Chandler School of Medicine and the Center on Aging, University of Kentucky, Lexington, KY, USA. hlevine@email.uky.edu

Abstract

Alzheimer's disease is defined pathologically by the presence of senile plaques, which consist primarily of extracellular aggregates of fibrillar Abeta peptide, and neurofibrillary tangles, which are abnormal, intracellular bundles of fibrillar tau protein. The advent of amyloid binding agents as diagnostic imaging probes for Alzheimer's disease (AD) has made it imperative to understand at a molecular and disease level what these ligands are reporting. In addition to improving the accuracy of diagnosis, we argue that these selective ligands can serve as probes for molecular polymorphisms that may govern the pathogenicity of abnormal protein aggregates.

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