Evidence map›Paper›PMID 34002449›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2022

Network dysfunction in cognitively normal APOE ε4 carriers is related to subclinical tau.

Omar H Butt, Karin L Meeker, Julie K Wisch, Suzanne E Schindler, Anne M Fagan, Tammie L S Benzinger, Carlos Cruchaga, David M Holtzman, John C Morris, Beau M Ances

Open access · greenAbstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Associations between Education Years and Resting-state Functional Connectivity Modulated byClinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Review
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 1 institution in 1 country.

Omar H ButtDepartment of Neurology, Washington University in Saint Louis, Saint Louis, Missouri, USA.ORCID 0000-0003-2252-3673
Karin L MeekerDepartment of Neurology, Washington University in Saint Louis, Saint Louis, Missouri, USA.
Julie K WischDepartment of Neurology, Washington University in Saint Louis, Saint Louis, Missouri, USA.
Suzanne E SchindlerDepartment of Neurology, Washington University in Saint Louis, Saint Louis, Missouri, USA.
Anne M FaganDepartment of Neurology, Washington University in Saint Louis, Saint Louis, Missouri, USA.
Tammie L S BenzingerDepartment of Radiology, Washington University in Saint Louis, Saint Louis, Missouri, USA.
Carlos CruchagaKnight Alzheimer Disease Research Center, Washington University in Saint Louis, St. Louis, Missouri, USA.
David M HoltzmanDepartment of Neurology, Washington University in Saint Louis, Saint Louis, Missouri, USA.
John C MorrisDepartment of Neurology, Washington University in Saint Louis, Saint Louis, Missouri, USA.
Beau M AncesDepartment of Neurology, Washington University in Saint Louis, Saint Louis, Missouri, USA.
Washington University in St. Louis · US

Funding

Smartphone-Based "Burst" Cognitive AssessmentsP01AG003991 · NIA · WASHINGTON UNIVERSITY · PI Tammie Lee Smith Benzinger · 1985 to 2026
$69.5M
WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
The natural history of AB accumulation in preclinical ADP01AG026276 · NIA · WASHINGTON UNIVERSITY · PI SCHINDLER, SUZANNE ELIZABETH · 2005 to 2025
$49.5M
Research Education ComponentP30AG066444 · NIA · WASHINGTON UNIVERSITY · PI DAVID M. HOLTZMAN · 2020 to 2026
$28.7M
NIA NIH HHS P01 AG003991NIA NIH HHS P01 AG026276NIA NIH HHS P30 AG066444NIA NIH HHS P50 AG005681
6 · The paper itself

Abstract

introductionApolipoprotein E (APOE) ε4 allele status is associated with amyloid and tau-related pathological changes related to Alzheimer's disease (AD). However, it is unknown whether brain network changes are related to amyloid beta (Aβ) and/or tau-related pathology in cognitively normal APOE ε4 carriers with subthreshold Aβ accumulation.

methodsResting state functional connectivity measures of network integrity were evaluated in cognitively normal individuals (n = 121, mean age 76.6 ± 7.8 years, 15% APOE ε4 carriers, 65% female) with minimal Aβ per cerebrospinal fluid (CSF) or amyloid positron emission tomography.

resultsAPOE ε4 carriers had increased lateralized connections relative to callosal connections within the default-mode, memory, and salience networks (P = .02), with significant weighting on linear regression toward CSF total tau (P = .03) and CSF phosphorylated tau at codon 181 (P = .03), but not CSF Aβ DISCUSSION: Cognitively normal APOE ε4 carriers with subthreshold amyloid accumulation may have network reorganization associated with tau.

Indexed as

Default Mode NetworkProdromal SymptomsAgedAlzheimer DiseaseAmyloidApolipoprotein E4BiomarkersBrainCognitionFemaleHeterozygoteHumansMagnetic Resonance ImagingMalePositron-Emission Tomographytau ProteinsAmyloidApolipoprotein E4Biomarkerstau Proteinsapolipoprotein Efunctional connectivitypreclinical Alzheimer's diseaseresting statetau

Identifiers

PMID34002449
PMCPMC8842835
OpenAlexW3161955916

What OpenQuestion holds

Textmetadata
LicenceTDM
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.