Evidence map›Paper›PMID 31492831›Full record

ArticleTranslational psychiatry2019

Drug repurposing for Alzheimer's disease based on transcriptional profiling of human iPSC-derived cortical neurons.

Gareth Williams, Ariana Gatt, Earl Clarke, Jonathan Corcoran, Patrick Doherty, David Chambers, Clive Ballard

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Integrative transcriptome-based drug repurposing in tuberculosis.bioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Article
  9. Drug repurposing in amyotrophic lateral sclerosis (ALS).Expert opinion on drug discovery · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Tackling neurodegenerationFrontiers in molecular neuroscience · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

7 authors at 2 institutions in 1 country.

Gareth WilliamsWolfson Centre for Age-Related Diseases, King's College London, London Bridge, London, SE1 1UL, UK. gareth.2.williams@kcl.ac.uk.
Ariana GattWolfson Centre for Age-Related Diseases, King's College London, London Bridge, London, SE1 1UL, UK.
Earl ClarkeWolfson Centre for Age-Related Diseases, King's College London, London Bridge, London, SE1 1UL, UK.
Jonathan CorcoranWolfson Centre for Age-Related Diseases, King's College London, London Bridge, London, SE1 1UL, UK.
Patrick DohertyWolfson Centre for Age-Related Diseases, King's College London, London Bridge, London, SE1 1UL, UK.
David ChambersWolfson Centre for Age-Related Diseases, King's College London, London Bridge, London, SE1 1UL, UK.
Clive BallardCollege of Medicine and Health, University of Exeter, Exeter, EX1 2LU, UK.
King's College London · GBUniversity of Exeter · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Alzheimer's disease is a complex disorder encompassing multiple pathological features with associated genetic and molecular culprits. However, target-based therapeutic strategies have so far proved ineffective. The aim of this study is to develop a methodology harnessing the transcriptional changes associated with Alzheimer's disease to develop a high content quantitative disease phenotype that can be used to repurpose existing drugs. Firstly, the Alzheimer's disease gene expression landscape covering severe disease stage, early pathology progression, cognitive decline and animal models of the disease has been defined and used to select a set of 153 drugs tending to oppose disease-associated changes in the context of immortalised human cancer cell lines. The selected compounds have then been assayed in the more biologically relevant setting of iPSC-derived cortical neuron cultures. It is shown that 51 of the drugs drive expression changes consistently opposite to those seen in Alzheimer's disease. It is hoped that the iPSC profiles will serve as a useful resource for drug repositioning within the context of neurodegenerative disease and potentially aid in generating novel multi-targeted therapeutic strategies.

Indexed as

Drug RepositioningInduced Pluripotent Stem CellsAlzheimer DiseaseHumansNeurons

Identifiers

PMID31492831
PMCPMC6731247
OpenAlexW2972250084

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.