Evidence map›Paper›PMID 29089479›Full record

ArticleNature communications2017

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, Oskar Hansson

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 588 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
588citing papers in PubMed, 1 pooled it
30.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

588 citing papers in PubMed, 1 synthesis or guideline pooled it, 910 citations in OpenAlex.

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  9. Excitation-inhibition imbalance links amyloid pathophysiology to cognition in non-demented individuals.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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528 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 3 countries.

Sebastian PalmqvistClinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Lund, Sweden. sebastian.palmqvist@med.lu.se.
Michael SchöllClinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-7800-1781
Olof StrandbergClinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Lund, Sweden.
Niklas MattssonClinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Lund, Sweden.
Erik StomrudClinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Lund, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemstry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemstry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Susan LandauHelen Wills Neuroscience Institute, University of California, Berkeley, USA.
William JagustHelen Wills Neuroscience Institute, University of California, Berkeley, USA.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Lund, Sweden. oskar.hansson@med.lu.se.
Lund University · SESahlgrenska University Hospital · SEUniversity of California, Berkeley · US

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
CIHRNIA NIH HHS U01 AG024904
6 · The paper itself

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.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesAtrophyBrainCohort StudiesFemaleGlucoseHumansMaleNerve NetOrgan SizeReproducibility of ResultsAmyloid beta-PeptidesGlucose

Identifiers

PMID29089479
PMCPMC5663717
OpenAlexW2766125374

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.