Evidence map›Paper›PMID 32426454›Full record

ArticleScience advances2020

Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive Tau PET in Alzheimer's disease.

Niklas Mattsson-Carlgren, Emelie Andersson, Shorena Janelidze, Rik Ossenkoppele, Philip Insel, Olof Strandberg, Henrik Zetterberg, Howard J Rosen, Gil Rabinovici, Xiyun Chai and 6 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
237citing papers in PubMed, 2 pooled it
24.9field-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

237 citing papers in PubMed, 2 syntheses or guidelines pooled it, 358 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The relationship of soluble tau species with Alzheimer's disease amyloid plaque removal and tau pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Trial
  4. Trial
  5. Trial
  6. Trial
  7. Article
  8. Article
  9. Excitation-inhibition imbalance links amyloid pathophysiology to cognition in non-demented individuals.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Classification of tau status with machine learning models in amyloid-positive cohorts.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  14. Article
  15. Encoding Discordance in the Alzheimer's Disease A/T/N Framework.medRxiv : the preprint server for health sciences · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

177 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

16 authors at 4 institutions in 4 countries.

Niklas Mattsson-CarlgrenClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.ORCID 0000-0002-8885-7724
Emelie AnderssonClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.
Shorena JanelidzeClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.
Rik OssenkoppeleClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.
Philip InselClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.
Olof StrandbergClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
Howard J RosenDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0001-9281-7402
Gil RabinoviciDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, USA.
Xiyun ChaiEli Lilly and Company, Indianapolis, IN, USA.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.ORCID 0000-0002-1890-4193
Jeffrey L DageEli Lilly and Company, Indianapolis, IN, USA.ORCID 0000-0002-2192-1699
Erik StomrudClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.ORCID 0000-0002-0841-5580
Ruben SmithClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.ORCID 0000-0001-7147-0112
Sebastian PalmqvistClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.
Oskar HanssonClinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.ORCID 0000-0001-8467-7286
Lund University · SEEli Lilly (United States) · USSahlgrenska University Hospital · SEUniversity of California, San Francisco · US

Funding

Technology and Remote Assessment CoreU19AG063911 · NIA · MAYO CLINIC ROCHESTER · PI Bradley F Boeve · 2019 to 2026
$120.9M
TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI BRUCE L MILLER · 2002 to 2026
$67.2M
Research Education ComponentP30AG062422 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HOWARD J ROSEN · 2019 to 2026
$36.9M
The Four Repeat Tauopathy Neuroimaging InitiativeR01AG038791 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2010 to 2020
$18.1M
Longitudinal Evaluation of Familial Frontotemporal Dementia Subjects (LEFFTDS)U01AG045390 · NIA · MAYO CLINIC ROCHESTER · PI BOEVE, BRADLEY F, ROSEN, HOWARD J · 2014 to 2018
$16.9M
Training - The Frontotemporal Lobar Degeneration Clinical Research ConsortiumU54NS092089 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2014 to 2018
$6.4M
Multimodal Imaging in Frontotemporal DegenerationK24AG045333 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSEN, HOWARD J · 2013 to 2023
$1.9M
NIA NIH HHS K24 AG045333NIA NIH HHS P01 AG019724NIA NIH HHS P30 AG062422NIA NIH HHS R01 AG038791NIA NIH HHS U01 AG045390NIA NIH HHS U19 AG063911NINDS NIH HHS U54 NS092089
6 · The paper itself

Abstract

The links between β-amyloid (Aβ) and tau in Alzheimer's disease are unclear. Cognitively unimpaired persons with signs of Aβ pathology had increased cerebrospinal fluid (CSF) phosphorylated tau (P-tau181 and P-tau217) and total-tau (T-tau), which increased over time, despite no detection of insoluble tau aggregates [normal Tau positron emission tomography (PET)]. CSF P-tau and T-tau started to increase before the threshold for Amyloid PET positivity, while Tau PET started to increase after Amyloid PET positivity. Effects of Amyloid PET on Tau PET were mediated by CSF P-tau, and high CSF P-tau predicted increased Tau PET rates. Individuals with

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBiomarkersMicePhosphorylationPositron-Emission Tomographytau ProteinsAmyloid beta-PeptidesBiomarkerstau Proteins

Identifiers

PMID32426454
PMCPMC7159908
OpenAlexW3016877536

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.