• Trends in neurosciences · Mar 2016

    Review

    BACE1 Physiological Functions May Limit Its Use as Therapeutic Target for Alzheimer's Disease.

    • Soraia Barão, Diederik Moechars, Stefan F Lichtenthaler, and Bart De Strooper.
    • VIB Center for the Biology of Disease, 3000 Leuven, Belgium; Center for Human Genetics, Universitaire Ziekenhuizen and LIND, KU Leuven, 3000 Leuven, Belgium.
    • Trends Neurosci. 2016 Mar 1; 39 (3): 158-169.

    AbstractThe protease β-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) is required for the production of the amyloid-β (Aβ) peptide, which is central to the pathogenesis of Alzheimer's disease (AD). Chronic inhibition of this protease may temper amyloid production and cure or prevent AD. However, while BACE1 inhibitors are being pushed forward as drug candidates, a remarkable gap in knowledge on the physiological functions of BACE1 and its close homolog BACE2 becomes apparent. Here we discuss the major discoveries of the past 3 years concerning BACE1 biology and to what extent these could limit the use of BACE1 inhibitors in the clinic. Copyright © 2016 Elsevier Ltd. All rights reserved.

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