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 and Oskar Hansson
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Niklas Mattsson: Clinical Memory Research Unit, Lund University
Philip S. Insel: Clinical Memory Research Unit, Lund University
Sebastian Palmqvist: Clinical Memory Research Unit, Lund University
Erik Stomrud: Clinical Memory Research Unit, Lund University
Danielle van Westen: Diagnostic Radiology, Lund University, Box 117
Lennart Minthon: Clinical Memory Research Unit, Lund University
Henrik Zetterberg: 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: Clinical Memory Research Unit, Lund University

Nature Communications, 2016, vol. 7, issue 1, 1-7

Abstract: Abstract Increased APP (amyloid precursor protein) processing causes β-amyloid (Aβ) accumulation in autosomal dominant Alzheimer's disease (AD), but it is unclear if it also affects sporadic Aβ accumulation. We tested healthy controls and patients with mild cognitive symptoms (N=331) in the BioFINDER study, using cerebrospinal fluid (CSF) Aβ40 as a surrogate for amyloidogenic APP processing. We find that levels of brain Aβ fibrils (measured by 18F-flutemetamol PET) are independently associated with high CSF Aβ40 (P

Date: 2016
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DOI: 10.1038/ncomms10918

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