Evidence map›Paper›PMID 34505023›Full record

ArticleEClinicalMedicine2021

High cerebrospinal amyloid-β 42 is associated with normal cognition in individuals with brain amyloidosis.

Andrea Sturchio, Alok K Dwivedi, Christina B Young, Tarja Malm, Luca Marsili, Jennifer S Sharma, Abhimanyu Mahajan, Emily J Hill, Samir El Andaloussi, Kathleen L Poston and 4 more

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

Article in EClinicalMedicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
12.5field-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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 124 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
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    Review
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  14. Review
  15. Article
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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

14 authors at 7 institutions in 3 countries.

Andrea SturchioJames J. and Joan A. Gardner Family Center for Parkinson's disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, OH, USA.
Alok K DwivediDivision of Biostatistics & Epidemiology, Department of Molecular and Translational Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA.
Christina B YoungDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Tarja MalmA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
Luca MarsiliJames J. and Joan A. Gardner Family Center for Parkinson's disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, OH, USA.
Jennifer S SharmaJames J. and Joan A. Gardner Family Center for Parkinson's disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, OH, USA.
Abhimanyu MahajanJames J. and Joan A. Gardner Family Center for Parkinson's disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, OH, USA.
Emily J HillJames J. and Joan A. Gardner Family Center for Parkinson's disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, OH, USA.
Samir El AndaloussiDepartment of Laboratory Medicine, Clinical Research Center, Karolinska Institutet, Stockholm, Sweden.
Kathleen L PostonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Fredric P ManfredssonDepartment of Neurobiology, Barrow Neurological Institute, Phoenix, AZ, USA.
Lon S SchneiderUniversity of Southern California Keck School of Medicine, Los Angeles, CA, USA.
Kariem EzzatDepartment of Laboratory Medicine, Clinical Research Center, Karolinska Institutet, Stockholm, Sweden.
Alberto J EspayJames J. and Joan A. Gardner Family Center for Parkinson's disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, OH, USA.
University of Cincinnati · USKarolinska Institutet · SEStanford University · USBarrow Neurological Institute · USTexas Tech University · USUniversity of Eastern Finland · FIUniversity of Southern California · US

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
USCADRC Diversity Supplement PachicanoP30AG066530 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HELENA Chang CHUI, ARTHUR W TOGA · 2020 to 2026
$27.8M
The Aging Brain: Vasculature, Ischemia, and BehaviorP01AG012435 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI REED, BRUCE · 1994 to 2012
$26.4M
NIA NIH HHS P01 AG012435NIA NIH HHS P30 AG066530NIA NIH HHS U01 AG024904
6 · The paper itself

Abstract

backgroundBrain amyloidosis does not invariably predict dementia. We hypothesized that high soluble 42-amino acid β amyloid (Aβ42) peptide levels are associated with normal cognition and hippocampal volume despite increasing brain amyloidosis.

methodsThis cross-sectional study of 598 amyloid-positive participants in the Alzheimer's Disease Neuroimaging Initiative cohort examined whether levels of soluble Aβ42 are higher in amyloid-positive normal cognition (NC) individuals compared to mild cognitive impairment (MCI) and Alzheimer's disease (AD) and whether this relationship applies to neuropsychological assessments and hippocampal volume measured within the same year. All subjects were evaluated between June 2010 and February 2019. Brain amyloid positivity was defined as positron emission tomography-based standard uptake value ratio (SUVR) ≥1.08 for

findingsHigher soluble Aβ42 levels were observed in NC (864.00 pg/ml) than in MCI (768.60 pg/ml) or AD (617.46 pg/ml), with the relationship between NC, MCI, and AD maintained across all amyloid tertiles. In adjusted analysis, there was a larger absolute effect size of soluble Aβ42 than SUVR for NC (0.82 vs. 0.40) and MCI (0.60 vs. 0.26) versus AD. Each standard deviation increase in Aβ42 was associated with greater odds of NC than AD (adjusted odds ratio, 6.26;

interpretationNormal cognition and hippocampal volume are associated with preservation of high soluble Aβ42 levels despite increasing brain amyloidosis.

fundingPlease refer to the Funding section at the end of the article.

Indexed as

Alzheimer's diseaseAtrophyHippocampusΒ-amyloid

Identifiers

PMID34505023
PMCPMC8413261
OpenAlexW3174935792

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.