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Neurotoxicity of the Alzheimer’s β-Amyloid Peptide

Spectroscopic and Microscopic Studies

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Bioimaging in Neurodegeneration

Part of the book series: Contemporary Neuroscience ((CNEURO))

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Abstract

Alzheimer’s disease (AD) is characterized pathologically by the presence in the brain of extracellular deposits of the β-amyloid or Abeta (Aβ) protein and intracellular neurofibrillary tangles composed of hyperphosphorylated tau. Molecular genetic data, largely based on familial AD patients, led to the “The Amyloid Hypothesis” being proposed, where the aggregation and deposition of Aβ is a pathogenic feature of the disease. The Aβ protein generally is described as a 39- to 43-amino acid peptide, although that barely hints at the complexities encountered in trying to understand the process by which it folds, aggregates, is deposited and, at some stage, is believed to bring about neuronal cell degeneration. This chapter, therefore, explores how many microscopic and spectroscopic techniques have been used in attempts to understand the Aβ fibrillization process and to provide a means of generating agents capable of halting Aβ deposition and hence disease progression in AD.

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Howlett, D.R. (2005). Neurotoxicity of the Alzheimer’s β-Amyloid Peptide. In: Broderick, P.A., Rahni, D.N., Kolodny, E.H. (eds) Bioimaging in Neurodegeneration. Contemporary Neuroscience. Humana Press. https://doi.org/10.1007/978-1-59259-888-5_6

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