Increased amyloidogenic APP processing in APOE ɛ4-negative individuals with cerebral β-amyloidosis

Niklas Mattsson; Philip S. Insel; Sebastian Palmqvist; Erik Stomrud; Danielle van Westen; Lennart Minthon; Henrik Zetterberg; Kaj Blennow; Oskar Hansson

doi:10.1038/ncomms10918

Nature Communications (Mar 2016)

Increased amyloidogenic APP processing in APOE ɛ4-negative individuals with cerebral β-amyloidosis

Niklas Mattsson,
Philip S. Insel,
Sebastian Palmqvist,
Erik Stomrud,
Danielle van Westen,
Lennart Minthon,
Henrik Zetterberg,
Kaj Blennow,
Oskar Hansson

Affiliations

Niklas Mattsson: Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University
Philip S. Insel: Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University
Sebastian Palmqvist: Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University
Erik Stomrud: Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University
Danielle van Westen: Department of Clinical Sciences, Diagnostic Radiology, Lund University, Box 117
Lennart Minthon: Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University
Henrik Zetterberg: Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square
Kaj Blennow: Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg
Oskar Hansson: Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University

DOI: https://doi.org/10.1038/ncomms10918
Journal volume & issue: Vol. 7, no. 1
pp. 1 – 7

Abstract

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Autosomal dominant Alzheimer's disease is thought to be caused by increased amyloidogenic APP processing. Mattson et al.show that association between brain Aβ and cerobrospinal fluid Aβ40 levels is stronger in APOE ɛ4 negative people, suggesting that increased processing may also underlie sporadic disease.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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