neurogenetics

, Volume 14, Issue 1, pp 1–9

Splice variants of the Alzheimer’s disease beta-secretase, BACE1

Authors

    • Laboratory of Molecular Neuroscience, Brain and Mind Research InstituteThe University of Sydney
    • Discipline of Biomedical Science, School of Medical Sciences, Sydney Medical SchoolThe University of Sydney
  • Nelleke Goense
    • Laboratory of Molecular Neuroscience, Brain and Mind Research InstituteThe University of Sydney
  • John Bohorquez
    • Laboratory of Molecular Neuroscience, Brain and Mind Research InstituteThe University of Sydney
  • Padraig Strappe
    • School of Biomedical SciencesCharles Sturt University
Review article

DOI: 10.1007/s10048-012-0348-3

Cite this article as:
Holsinger, R.M.D., Goense, N., Bohorquez, J. et al. Neurogenetics (2013) 14: 1. doi:10.1007/s10048-012-0348-3

Abstract

Cleavage of the amyloid precursor protein by enzymes commonly referred to as β- and γ-secretase constitute an important process in the pathogenesis of Alzheimer’s disease (AD). The regulation of this process is therefore an important subject of investigation. Numerous sources of endogenous regulation have been identified, and one of these is the relative abundance and regulation of splice variants of the β-secretase, BACE1 (β-site amyloid precursor protein cleaving enzyme 1). In this review, we will briefly discuss the main characteristics of BACE1, review the different variants of this enzyme that have been identified to date, and highlight their possible implication in AD.

Keywords

Amyloid precursor protein Amyloid beta Endogenous regulation Enzyme activity Glycosylation Molecular characterization

Copyright information

© Springer-Verlag Berlin Heidelberg 2012