neurogenetics

, Volume 14, Issue 1, pp 1–9

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

  • R. M. Damian Holsinger
  • Nelleke Goense
  • John Bohorquez
  • Padraig Strappe
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
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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 proteinAmyloid betaEndogenous regulationEnzyme activityGlycosylationMolecular characterization

Copyright information

© Springer-Verlag Berlin Heidelberg 2012

Authors and Affiliations

  • R. M. Damian Holsinger
    • 1
    • 2
  • Nelleke Goense
    • 1
  • John Bohorquez
    • 1
  • Padraig Strappe
    • 3
  1. 1.Laboratory of Molecular Neuroscience, Brain and Mind Research InstituteThe University of SydneyCamperdownAustralia
  2. 2.Discipline of Biomedical Science, School of Medical Sciences, Sydney Medical SchoolThe University of SydneyLidcombeAustralia
  3. 3.School of Biomedical SciencesCharles Sturt UniversityWagga WaggaAustralia