Evidence map›Paper›PMID 38102482›Full record

ArticleMolecular psychiatry2024

Cerebral organoids with chromosome 21 trisomy secrete Alzheimer's disease-related soluble aggregates detectable by single-molecule-fluorescence and super-resolution microscopy.

Emre Fertan, Dorothea Böken, Aoife Murray, John S H Danial, Jeff Y L Lam, Yunzhao Wu, Pollyanna A Goh, Ivan Alić, Matthew R Cheetham, Evgeniia Lobanova and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Small-diffusible aggregates, plaques, tangles, and dynamic equilibria: Untangling Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  10. Lecanemab preferentially binds to smaller aggregates present at early Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  11. Article
  12. Article
  13. Article
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

13 authors at 2 institutions in 3 countries.

Emre FertanYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, CB2 1EW, UK.
Dorothea BökenYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, CB2 1EW, UK.
Aoife MurrayThe Blizard Institute, Barts & The London School of Medicine, Queen Mary University of London, London, E1 2AT, UK.ORCID 0000-0002-4780-3957
John S H DanialYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, CB2 1EW, UK.
Jeff Y L LamYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, CB2 1EW, UK.
Yunzhao WuYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, CB2 1EW, UK.
Pollyanna A GohThe Blizard Institute, Barts & The London School of Medicine, Queen Mary University of London, London, E1 2AT, UK.
Ivan AlićThe Blizard Institute, Barts & The London School of Medicine, Queen Mary University of London, London, E1 2AT, UK.ORCID 0000-0002-8125-8198
Matthew R CheethamYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, CB2 1EW, UK.
Evgeniia LobanovaYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, CB2 1EW, UK.
Yu P ZhangYusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, CB2 1EW, UK.
Dean Nižetić *The Blizard Institute, Barts & The London School of Medicine, Queen Mary University of London, London, E1 2AT, UK.ORCID 0000-0001-5486-5761
David Klenerman *Yusuf Hamied Department of Chemistry, University of Cambridge, Cambridge, CB2 1EW, UK. dk10012@cam.ac.uk.ORCID 0000-0001-7116-6954
University of Cambridge · GBQueen Mary University of London · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Understanding the role of small, soluble aggregates of beta-amyloid (Aβ) and tau in Alzheimer's disease (AD) is of great importance for the rational design of preventative therapies. Here we report a set of methods for the detection, quantification, and characterisation of soluble aggregates in conditioned media of cerebral organoids derived from human iPSCs with trisomy 21, thus containing an extra copy of the amyloid precursor protein (APP) gene. We detected soluble beta-amyloid (Aβ) and tau aggregates secreted by cerebral organoids from both control and the isogenic trisomy 21 (T21) genotype. We developed a novel method to normalise measurements to the number of live neurons within organoid-conditioned media based on glucose consumption. Thus normalised, T21 organoids produced 2.5-fold more Aβ aggregates with a higher proportion of larger (300-2000 nm

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesDown SyndromeInduced Pluripotent Stem CellsOrganoidstau ProteinsAmyloid beta-Protein PrecursorBrainCarrier ProteinsCulture Media, ConditionedHumansMicroscopy, FluorescenceNeuronsOxidative StressPlaque, AmyloidTrisomyAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCarrier ProteinsCulture Media, Conditionedtau ProteinsTXNIP protein, human

Identifiers

PMID38102482
PMCPMC11116105
OpenAlexW4389816879

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Registered trials

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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.