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Serum Starvation Induces BACE1 Processing and Secretion.

A V Stavropoulou1, O Mavrofrydi1, P Saftig2

  • 1Division of Human and Animal Physiology, Department of Biology, National and Kapodistrian University of Athens, Athens, Greece.

Current Alzheimer Research
|October 28, 2016
PubMed
Summary

Serum deprivation triggers the secretion of beta-secretase (BACE1) in cells. This shedding is mediated by ADAM10, an enzyme, and may contribute to Alzheimer's disease pathogenesis.

Keywords:
ADAM10ADAM17Alzheimer's diseaseBACE1cholesterolproteolysissecretionserum starvation.shedding

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Beta-secretase (BACE1) is crucial in Alzheimer's Disease (AD) pathogenesis.
  • BACE1 cleaves Amyloid Precursor Protein (APP), leading to toxic Aβ peptide formation.
  • Elevated BACE1 levels in CSF of AD patients suggest neurodegeneration induces BACE1 shedding.

Purpose of the Study:

  • To investigate if serum deprivation stimulates proteolysis-dependent BACE1 secretion.
  • To mimic in vitro conditions that may lead to BACE1 shedding.

Main Methods:

  • BACE1 secretion was detected in BACE1-overexpressing cells under serum deprivation using western blot.
  • ADAM10/ADAM17 knockout fibroblasts and inhibitors were used to identify involved proteases.
  • Cellular localization and membrane lipid composition changes were analyzed.

Main Results:

  • Serum deprivation stimulated BACE1 secretion in neuroblastoma and HEK293T cells.
  • ADAM10 and ADAM17 proteases were implicated in serum-starvation-induced BACE1 shedding.
  • Cholesterol depletion potentiated BACE1 shedding, suggesting membrane lipid alterations are involved.
  • Secreted BACE1 retained enzymatic activity towards full-length APP.

Conclusions:

  • Serum starvation induces BACE1 secretion.
  • ADAM10 is the primary protease responsible for this shedding.
  • Altered membrane lipid composition may facilitate BACE1 and ADAM10 interaction.