Evidence map›Paper›PMID 32942175›Full record

ArticleNeuroImage. Clinical2020

Resting-state functional connectivity and amyloid burden influence longitudinal cortical thinning in the default mode network in preclinical Alzheimer's disease.

Olivia L Hampton, Rachel F Buckley, Lyssa K Manning, Matthew R Scott, Michael J Properzi, Cleofé Peña-Gómez, Heidi I L Jacobs, Jasmeer P Chhatwal, Keith A Johnson, Reisa A Sperling and 1 more

Open access · goldAbstract read
In one paragraph

Article in NeuroImage. Clinical, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  6. Sex-specific topological structure associated with dementia via latent space estimation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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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

11 authors at 3 institutions in 3 countries.

Olivia L HamptonDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA.
Rachel F BuckleyDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA; Melbourne School of Psychological Science, University of Melbourne, VIC 3010, Australia; Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA.
Lyssa K ManningDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA.
Matthew R ScottDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA.
Michael J ProperziDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA.
Cleofé Peña-GómezDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA.
Heidi I L JacobsDepartment of Radiology, Massachusetts General Hospital/Harvard Medical School, Boston 02114, MA, USA; Faculty of Health, Medicine and Life Sciences, School for Mental Health and Neuroscience, Alzheimer Centre Limburg, Maastricht University, Maastricht 6200, The Netherlands.
Jasmeer P ChhatwalDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA; Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA.
Keith A JohnsonDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Radiology, Massachusetts General Hospital/Harvard Medical School, Boston 02114, MA, USA.
Reisa A SperlingDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA; Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA.
Aaron P SchultzDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Radiology, Massachusetts General Hospital/Harvard Medical School, Boston 02114, MA, USA. Electronic address: apschultz@mgh.harvard.edu.
Massachusetts General Hospital · USHarvard University · USBrigham and Women's Hospital · US

Funding

Vascular factors, physical activity, and inflammation as modulators of neurodegenerative and cognitive trajectories (Project 2)P01AG036694 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Rachel Frances Buckley · 2010 to 2026
$50.2M
Project 4P41EB015896 · NIBIB · MASSACHUSETTS GENERAL HOSPITAL · PI ROSEN, BRUCE R · 2012 to 2018
$9.8M
A Storage Area Network for Structural and Functional Image AnalysisS10RR023401 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI FISCHL, BRUCE · 2009 to 2009
$2.0M
SILICON GRAPHICS PRISM EXTREME 128P/1TBS10RR023043 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI SORENSEN, ALMA GREGORY · 2006 to 2006
$1.5M
Mentoring Imaging Research in Early ADK24AG035007 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI SPERLING, REISA A. · 2010 to 2020
$1.4M
A Siemens MAGNETOTOM Trio 3 Tesla MRI SystemS10RR021110 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI ROSEN, BRUCE R · 2006 to 2006
$500k
A 3.0 Tesla MRI System in a Neuroscience ICUS10RR019254 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI SORENSEN, ALMA GREGORY · 2004 to 2004
$500k
Computeserver Structural &Functional Image AnalysisS10RR019307 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI FISCHL, BRUCE · 2004 to 2004
$496k
NCRR NIH HHS S10 RR019254NCRR NIH HHS S10 RR019307NCRR NIH HHS S10 RR021110NCRR NIH HHS S10 RR023043NCRR NIH HHS S10 RR023401NIA NIH HHS K24 AG035007NIA NIH HHS P01 AG036694NIBIB NIH HHS P41 EB015896
6 · The paper itself

Abstract

Proteinopathies are key elements in the pathogenesis of age-related neurodegenerative diseases, particularly Alzheimer's disease (AD), with the nature and location of the proteinopathy characterizing much of the disease phenotype. Susceptibility of brain regions to pathology may partly be determined by intrinsic network structure and connectivity. It remains unknown, however, how these networks inform the disease cascade in the context of AD biomarkers, such as beta-amyloid (Aβ), in clinically-normal older adults.The default-mode network (DMN), a prominent intrinsic network, is heavily implicated in AD due to its spatial overlap with AD atrophy patterns and tau deposition. We investigated the influence of baseline Aβ positron emission tomography (PET) signal and intrinsic DMN connectivity on DMN-specific cortical thinning in 120 clinically-normal older adults from the Harvard Aging Brain Study (73 ± 6 years, 58% Female, CDR = 0). Participants underwent

Indexed as

Alzheimer DiseaseAgedAmyloid beta-PeptidesBrainCerebral Cortical ThinningDefault Mode NetworkFemaleHumansMagnetic Resonance ImagingMalePositron-Emission TomographyTomography, X-Ray ComputedAmyloid beta-PeptidesAlzheimer’s diseaseAmyloidDefault mode networkFunctional connectivity

Identifiers

PMID32942175
PMCPMC7498941
OpenAlexW3082963664

What OpenQuestion holds

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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.