Abstract
The amyloidogenic fragment βA4 is derived from a larger precursor, the amyloid precursor protein (APP), which is normally expressed in the brain as a larger transmembrane glycoprotein which can be subject to several cleavage events and secreted. The predominant processing pathway cleaves APP within the βA4 peptide sequence, while other events can result in minor quantities of βA4. Thus it is believed that the accumulation of βA4 results from one or several errors in the normal metabolism of its precursor (for review, see Selkoe et al. 1994). However, the normal physiological function of APP and its trafficking remains to be elucidated.
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© 1995 Springer-Verlag Berlin Heidelberg
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Allinquant, B., Hantraye, P., Bouillot, C., Moya, K.L., Prochiantz, A. (1995). Implication of the Amyloid Precursor Protein in Neurite Outgrowth. In: Kosik, K.S., Selkoe, D.J., Christen, Y. (eds) Alzheimer’s Disease: Lessons from Cell Biology. Research and Perspectives in Alzheimer’s Disease. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79423-0_6
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DOI: https://doi.org/10.1007/978-3-642-79423-0_6
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