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

Journal article
Authors Sebastian Palmqvist
Michael Schöll
Olof Strandberg
Niklas Mattsson
Erik Stomrud
Henrik Zetterberg
Kaj Blennow
Susan Landau
William Jagust
Oskar Hansson
Published in Nature communications
Volume 8
Issue 1
ISSN 2041-1723
Publication year 2017
Published at Institute of Neuroscience and Physiology
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Language en
Links dx.doi.org/10.1038/s41467-017-01150...
www.ncbi.nlm.nih.gov/entrez/query.f...
Subject categories Neurosciences, Neurology, Radiology, Nuclear Medicine and Medical Imaging

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.

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