Abstract
Theβ-amyloid peptide (Aβ), the major component of the neuritic plaques characterizing Alzheimer’s disease (AD), is a 39 to 43 amino acid peptide derived from proteolytic cleavage of a larger β-amyloid precursor protein (APP). Mutations in the APP gene have been identified which cause familial, early onset AD, suggesting that APP metabolism is a central event in AD progression (Mullan & Crawford, 1993). APP is an abundant protein in the brain and Aβ is produced not only in AD patients, but also in cerebrospinal fluid (CSF) of normal individuals (Selkoe, 1994). APP has been implicated in numerous activities based on in vitro studies, such as regulation of cell adhesion, neurite outgrowth and intraneuronal calcium (Selkoe, 1994). However, the in vivo function of APP remains unclear.
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© 1997 Birkhäuser Boston
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Zheng, H. et al. (1997). APP Knockout and APP Over-Expression in Transgenic Mice. In: Becker, R.E., Giacobini, E., Barton, J.M., Brown, M. (eds) Alzheimer Disease. Advances in Alzheimer Disease Therapy. Birkhäuser Boston. https://doi.org/10.1007/978-1-4612-4116-4_21
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DOI: https://doi.org/10.1007/978-1-4612-4116-4_21
Publisher Name: Birkhäuser Boston
Print ISBN: 978-1-4612-8660-8
Online ISBN: 978-1-4612-4116-4
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