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Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

The pathological hallmarks of Alzheimer’s disease (AD) are senile plaques and neurofibrillary tangles. A major component of senile plaque is β-amyloid peptide (Aβ) [1 2]. Several lines of evidence suggest that a progressive deposition of aggregated Aβ is an early and necessary event in AD [3-5]. Several forms of the hydrophobic Aβ, consisting of 39-43 amino acids, are generated from the amyloid precursor protein (APP) [3-5]. Synthetic Aβ spontaneously aggregates and forms amyloid-like fibril [6 7]. The aggregated Aβ is neurotoxic [8 9].

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Tooyama, I. (2001). Interactions of α2-macroglobulin and amyloid β peptide. In: Rogers, J. (eds) Neuroinflammatory Mechanisms in Alzheimer’s Disease Basic and Clinical Research. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8350-4_7

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  • DOI: https://doi.org/10.1007/978-3-0348-8350-4_7

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