Evidence map›Paper›PMID 39187705›Full record

ArticleNature neuroscience2024

Proteomic changes in Alzheimer's disease associated with progressive Aβ plaque and tau tangle pathologies.

Alexa Pichet Binette, Chris Gaiteri, Malin Wennström, Atul Kumar, Ines Hristovska, Nicola Spotorno, Gemma Salvadó, Olof Strandberg, Hansruedi Mathys, Li-Huei Tsai and 6 more

Abstract read
In one paragraph

Article in Nature neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
–field-weighted citation impact
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

101 citing papers in PubMed.

  1. Gut microbes · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Tau-PET and CSF MTBR-tau243 comparisons validate increased tau aggregation in females.European journal of nuclear medicine and molecular imaging · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Blood-based proteomic signature of amyloidosis: identification of novel regulators of amyloid load.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  17. Review
  18. Review
  19. Review
  20. Article

41 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.

Alexa Pichet BinetteClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden. alexa.pichet_binette@med.lu.se.ORCID http://orcid.org/0000-0001-5218-3337
Chris GaiteriDepartment of Psychiatry, SUNY Upstate Medical University, Syracuse, NY, USA.
Malin WennströmCognitive Disorder Research Unit, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Atul KumarClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Ines HristovskaClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Nicola SpotornoClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Gemma SalvadóClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-5210-9230
Olof StrandbergClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Hansruedi MathysPicower Institute for Learning and Memory, MIT, Cambridge, MA, USA.ORCID http://orcid.org/0000-0003-0186-2115
Li-Huei TsaiPicower Institute for Learning and Memory, MIT, Cambridge, MA, USA.ORCID http://orcid.org/0000-0003-1262-0592
Sebastian PalmqvistClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-9267-1930
Niklas Mattsson-CarlgrenClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Shorena JanelidzeClinical 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.
Jacob W VogelDepartment of Clinical Sciences Malmö, SciLifeLab, Lund University, Lund, Sweden.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden. oskar.hansson@med.lu.se.ORCID http://orcid.org/0000-0001-8467-7286

Funding

Cell type specific epigenetic analysis to understand complex mechanisms underlying Alzheimer's disease phenotypesRF1AG054012 · NIA · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KELLIS, MANOLIS, TSAI, LI-HUEI · 2016 to 2016
$3.9M
Dissection of endosomal trafficking mechanisms in Alzheimer's DiseaseRF1AG062377 · NIA · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI TSAI, LI-HUEI · 2018 to 2018
$3.6M
BrightFocus Foundation (BrightFocus) A2021013FFonds de Recherche du Québec - Santé (Fonds de la recherche en sante du Quebec) 298314NIA NIH HHS RF1 AG054012NIA NIH HHS RF1 AG062377Vetenskapsrådet (Swedish Research Council) 2022-00775
6 · The paper itself

Abstract

Proteomics can shed light on the dynamic and multifaceted alterations in neurodegenerative disorders like Alzheimer's disease (AD). Combining radioligands measuring β-amyloid (Aβ) plaques and tau tangles with cerebrospinal fluid proteomics, we uncover molecular events mirroring different stages of AD pathology in living humans. We found 127 differentially abundant proteins (DAPs) across the AD spectrum. The strongest Aβ-related proteins were mainly expressed in glial cells and included SMOC1 and ITGAM. A dozen proteins linked to ATP metabolism and preferentially expressed in neurons were independently associated with tau tangle load and tau accumulation. Only 20% of the DAPs were also altered in other neurodegenerative diseases, underscoring AD's distinct proteome. Two co-expression modules related, respectively, to protein metabolism and microglial immune response encompassed most DAPs, with opposing, staggered trajectories along the AD continuum. We unveil protein signatures associated with Aβ and tau proteinopathy in vivo, offering insights into complex neural responses and potential biomarkers and therapeutics targeting different disease stages.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesNeurofibrillary TanglesPlaque, AmyloidProteomicstau ProteinsAgedAged, 80 and overBiomarkersBrainFemaleHumansMaleProteomeAmyloid beta-PeptidesBiomarkersProteometau Proteins

Identifiers

PMID39187705
PMCPMC11452344

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.