Evidence map›Paper›PMID 39704342›Full record

ArticleStem cells (Dayton, Ohio)2025

Changes in iPSC-astrocyte morphology reflect Alzheimer's disease patient clinical markers.

Helen A Rowland, Georgina Miller, Qiang Liu, Shuhan Li, Nicola R Sharp, Bryan Ng, Tina Wei, Kanisa Arunasalam, Ivan Koychev, Anne Hedegaard and 17 more

Abstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Astrocytic KFrontiers in aging neuroscience · 2026
    Review
  3. Article
  4. Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

27 authors.

Helen A RowlandDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Georgina MillerDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Qiang LiuDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Shuhan LiDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Nicola R SharpDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Bryan NgKavli Institute for Nanoscience Discovery, University of Oxford, Oxford OX1 3QU, United Kingdom.
Tina WeiKavli Institute for Nanoscience Discovery, University of Oxford, Oxford OX1 3QU, United Kingdom.
Kanisa ArunasalamNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX1 3QU, United Kingdom.
Ivan KoychevDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.ORCID 0000-0001-6813-8493
Anne HedegaardDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Elena M RibeDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Dennis ChanDepartment of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
Tharani ChessellNeuroscience, BioPharmaceuticals R&D, AstraZeneca, Granta Park, Cambridge CB21 6GH, United Kingdom.
Ece KocagoncuMedical Research Council Cognition and Brain Sciences Unit, Department of Clinical Neurosciences and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge CB2 7EF, United Kingdom.
Jennifer LawsonDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Paresh MalhotraDepartment of Brain Sciences, Imperial College London, London W6 8RP, United Kingdom.
Basil H RidhaDementia Research Centre, UCL Institute of Neurology, London WC1N 3BG, United Kingdom.ORCID 0000-0002-8850-9922
James B RoweMedical Research Council Cognition and Brain Sciences Unit, Department of Clinical Neurosciences and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge CB2 7EF, United Kingdom.
Alan J ThomasTranslational and Clinical Research Institute, Newcastle University, Newcastle, United Kingdom.
Giovanna ZamboniNuffield Department of Clinical Neurosciences, Headington, University of Oxford, Oxford OX3 9DS, United Kingdom.ORCID 0000-0002-6133-3373
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, S-431 80 Mölndal, Sweden.ORCID 0000-0003-3930-4354
M Zameel CaderKavli Institute for Nanoscience Discovery, University of Oxford, Oxford OX1 3QU, United Kingdom.ORCID 0000-0002-6952-406X
Richard Wade-MartinsKavli Institute for Nanoscience Discovery, University of Oxford, Oxford OX1 3QU, United Kingdom.
Simon LovestoneDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Alejo Nevado-HolgadoDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Andrey KormilitzinDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.
Noel J BuckleyDepartment of Psychiatry, University of Oxford, Headington, Oxford OX3 7JX, United Kingdom.ORCID 0000-0003-1152-0653

Funding

Medical Research Council MC_EX_MR/N50192X/1Medical Research Council MR/L023784/2Medical Research Council MR/M024962/1Medical Research Council MR/N029941/1Medical Research Council Dementias Platform UK Experimental Medicine Award MR/M024962/1National Institute for Health Research
6 · The paper itself

Abstract

Human induced pluripotent stem cells (iPSCs) provide powerful cellular models of Alzheimer's disease (AD) and offer many advantages over non-human models, including the potential to reflect variation in individual-specific pathophysiology and clinical symptoms. Previous studies have demonstrated that iPSC-neurons from individuals with Alzheimer's disease (AD) reflect clinical markers, including β-amyloid (Aβ) levels and synaptic vulnerability. However, despite neuronal loss being a key hallmark of AD pathology, many risk genes are predominantly expressed in glia, highlighting them as potential therapeutic targets. In this work iPSC-derived astrocytes were generated from a cohort of individuals with high versus low levels of the inflammatory marker YKL-40, in their cerebrospinal fluid (CSF). iPSC-derived astrocytes were treated with exogenous Aβ oligomers and high content imaging demonstrated a correlation between astrocytes that underwent the greatest morphology change from patients with low levels of CSF-YKL-40 and more protective APOE genotypes. This finding was subsequently verified using similarity learning as an unbiased approach. This study shows that iPSC-derived astrocytes from AD patients reflect key aspects of the pathophysiological phenotype of those same patients, thereby offering a novel means of modelling AD, stratifying AD patients and conducting therapeutic screens.

Indexed as

Alzheimer DiseaseAstrocytesInduced Pluripotent Stem CellsAgedAmyloid beta-PeptidesApolipoproteins EBiomarkersChitinase-3-Like Protein 1FemaleHumansMaleAmyloid beta-PeptidesApolipoproteins EBiomarkersCHI3L1 protein, humanChitinase-3-Like Protein 1astrocytedeep learningmorphologystem cellYKL-40

Identifiers

PMID39704342
PMCPMC11907432

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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.