Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity

Sebastian Palmqvist (), Michael Schöll, Olof Strandberg, Niklas Mattsson, Erik Stomrud, Henrik Zetterberg, Kaj Blennow, Susan Landau, William Jagust and Oskar Hansson ()
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Sebastian Palmqvist: Malmö, Lund University
Michael Schöll: Malmö, Lund University
Olof Strandberg: Malmö, Lund University
Niklas Mattsson: Malmö, Lund University
Erik Stomrud: Malmö, Lund University
Henrik Zetterberg: the Sahlgrenska Academy at the University of Gothenburg
Kaj Blennow: the Sahlgrenska Academy at the University of Gothenburg
Susan Landau: University of California
William Jagust: University of California
Oskar Hansson: Malmö, Lund University

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract It is not known exactly where amyloid-β (Aβ) fibrils begin to accumulate in individuals with Alzheimer’s disease (AD). Recently, we showed that abnormal levels of Aβ42 in cerebrospinal fluid (CSF) can be detected before abnormal amyloid can be detected using PET in individuals with preclinical AD. Using these approaches, here we identify the earliest preclinical AD stage in subjects from the ADNI and BioFINDER cohorts. We show that Aβ accumulation preferentially starts in the precuneus, medial orbitofrontal, and posterior cingulate cortices, i.e., several of the core regions of the default mode network (DMN). This early pattern of Aβ accumulation is already evident in individuals with normal Aβ42 in the CSF and normal amyloid PET who subsequently convert to having abnormal CSF Aβ42. The earliest Aβ accumulation is further associated with hypoconnectivity within the DMN and between the DMN and the frontoparietal network, but not with brain atrophy or glucose hypometabolism. Our results suggest that Aβ fibrils start to accumulate predominantly within certain parts of the DMN in preclinical AD and already then affect brain connectivity.

Date: 2017
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DOI: 10.1038/s41467-017-01150-x

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