Abstract
Aggregation and precipitation of peptides appear to play a major role in neurodegenerative diseases such as Alzheimer’s disease (AD) (Teplow 1998), Parkinson’s disease (Mezey et al. 1998), and Huntington’s disease (Georgalis et al. 1998). In AD, the aggregating Amyloid β-peptide (Aβ) accumulates in highly insoluble senile plaques, which are the defining pathological symptoms of the disease (Selkoe 1996). Aβ is derived by proteolytic processing from the β-Amyloid precursor protein βAPP; Selkoe 1996). Two secretases have been postulated, which either generate the N-terminus (β-secretale) or the C-terminus (γ-secretase) of Aβ (Haass and Selkoe 1993; Fig. 1). Aβ is produced under physiological conditions in cultured cells and is secreted into the media. In vivo, Aβ is detected in human plasma and cerebrospinal fluid (Haass and Selkoe 1993).
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Haass, C. (2000). Presenilin Proteins and Their Function During Embryonic Development and Alzheimer’s Disease. In: Nüsslein-Volhard, C., Krätzschmar, J. (eds) Of Fish, Fly, Worm, and Man. Ernst Schering Research Foundation Workshop, vol 29. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-04264-9_4
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DOI: https://doi.org/10.1007/978-3-662-04264-9_4
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