Nature Communications (May 2019)
Aβ34 is a BACE1-derived degradation intermediate associated with amyloid clearance and Alzheimer’s disease progression
- Filip Liebsch,
- Luka Kulic,
- Charlotte Teunissen,
- Adeola Shobo,
- Irem Ulku,
- Vivienne Engelschalt,
- Mark A. Hancock,
- Wiesje M. van der Flier,
- Peter Kunach,
- Pedro Rosa-Neto,
- Philip Scheltens,
- Judes Poirier,
- Paul Saftig,
- Randall J. Bateman,
- John Breitner,
- Christoph Hock,
- Gerhard Multhaup
Affiliations
- Filip Liebsch
- Department of Pharmacology and Therapeutics and Integrated Program in Neuroscience, McGill University
- Luka Kulic
- Institute for Regenerative Medicine, University of Zurich
- Charlotte Teunissen
- Department of Clinical Chemistry, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam
- Adeola Shobo
- Department of Pharmacology and Therapeutics and Integrated Program in Neuroscience, McGill University
- Irem Ulku
- Department of Pharmacology and Therapeutics and Integrated Program in Neuroscience, McGill University
- Vivienne Engelschalt
- Institut für Chemie und Biochemie, Freie Universität Berlin
- Mark A. Hancock
- SPR-MS Facility, McGill University
- Wiesje M. van der Flier
- Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam
- Peter Kunach
- Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Alzheimer’s Disease Research Unit, Douglas Research Institute, McGill University
- Pedro Rosa-Neto
- Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Alzheimer’s Disease Research Unit, Douglas Research Institute, McGill University
- Philip Scheltens
- Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam
- Judes Poirier
- Department of Psychiatry, McGill University
- Paul Saftig
- Biochemisches Institut, Christian-Albrechts-Universität-Kiel
- Randall J. Bateman
- Department of Neurology, Washington University in St. Louis
- John Breitner
- Department of Psychiatry, McGill University
- Christoph Hock
- Institute for Regenerative Medicine, University of Zurich
- Gerhard Multhaup
- Department of Pharmacology and Therapeutics and Integrated Program in Neuroscience, McGill University
- DOI
- https://doi.org/10.1038/s41467-019-10152-w
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 15
Abstract
Aβ34 is generated from degradation of Aβ40 and Aβ42 by β-secretase. Here, the authors show that Aβ34 is a marker for amyloid clearance and is elevated in the CSF of patients that go on to convert from mild cognitive impairment to Alzheimer’s disease, suggesting it may be a useful biomarker.
