Evidence map›Paper›PMID 28966121›Full record

ArticleStem cell reports2017

Scalable Production of iPSC-Derived Human Neurons to Identify Tau-Lowering Compounds by High-Content Screening.

Chao Wang, Michael E Ward, Robert Chen, Kai Liu, Tara E Tracy, Xu Chen, Min Xie, Peter Dongmin Sohn, Connor Ludwig, Anke Meyer-Franke and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 249 papers.

0numbers the graph read from it
0cells of the map it votes in
249citing papers in PubMed
25.8field-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

249 citing papers in PubMed, 449 citations in OpenAlex.

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  18. PrPStem cell reports · 2026
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189 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

13 authors at 4 institutions in 1 country.

Chao WangGladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA.
Michael E WardGladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA; National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, Bethesda, MD 20892, USA.
Robert ChenDepartment of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA.
Kai LiuGladstone Institute of Cardiovascular Disease, 1650 Owens Street, San Francisco, CA 94158, USA; Department of Pharmaceutical Chemistry, University of California, San Francisco, 600 16th Street, San Francisco, CA 94158, USA.
Tara E TracyGladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA.
Xu ChenGladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA.
Min XieGladstone Institute of Cardiovascular Disease, 1650 Owens Street, San Francisco, CA 94158, USA; Department of Pharmaceutical Chemistry, University of California, San Francisco, 600 16th Street, San Francisco, CA 94158, USA.
Peter Dongmin SohnGladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA.
Connor LudwigDepartment of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA.
Anke Meyer-FrankeGladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA.
Celeste M KarchDepartment of Psychiatry, Washington University School of Medicine, 425 South Euclid Avenue, St. Louis, MO 63110, USA.
Sheng DingGladstone Institute of Cardiovascular Disease, 1650 Owens Street, San Francisco, CA 94158, USA; Department of Pharmaceutical Chemistry, University of California, San Francisco, 600 16th Street, San Francisco, CA 94158, USA.
Li GanGladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA. Electronic address: lgan@gladstone.ucsf.edu.
Gladstone Institutes · USUniversity of California, San Francisco · USNational Institute of Neurological Disorders and Stroke · USWashington University in St. Louis · US

Funding

Mechanisms of inherited neurodegenerative diseasesZIANS003155 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI WARD, MICHAEL · 2016 to 2025
$24.7M
Molecular mechanisms in progranulin deficient frontotemporal dementiaR01AG051390 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI GAN, LI · 2015 to 2019
$2.5M
SIRT1 Limits Microglial Toxicity in Alzheimer's DiseaseR01AG036884 · NIA · J. DAVID GLADSTONE INSTITUTES · PI GAN, LI · 2012 to 2016
$2.0M
GENETIC DISRUPTION OF TAU METABOLISM IN TAUOPATHIESK01AG046374 · NIA · WASHINGTON UNIVERSITY · PI KARCH, CELESTE MARIE · 2014 to 2018
$568k
Investigation of nuclear transport dysfunction in an ocular model of FTLDK08EY023610 · NEI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WARD, MICHAEL EMMERSON · 2013 to 2015
$486k
NEI NIH HHS K08 EY023610NIA NIH HHS K01 AG046374NIA NIH HHS R01 AG036884NIA NIH HHS R01 AG051390
6 · The paper itself

Abstract

Lowering total tau levels is an attractive therapeutic strategy for Alzheimer's disease and other tauopathies. High-throughput screening in neurons derived from human induced pluripotent stem cells (iPSCs) is a powerful tool to identify tau-targeted therapeutics. However, such screens have been hampered by heterogeneous neuronal production, high cost and low yield, and multi-step differentiation procedures. We engineered an isogenic iPSC line that harbors an inducible neurogenin 2 transgene, a transcription factor that rapidly converts iPSCs to neurons, integrated at the AAVS1 locus. Using a simplified two-step protocol, we differentiated these iPSCs into cortical glutamatergic neurons with minimal well-to-well variability. We developed a robust high-content screening assay to identify tau-lowering compounds in LOPAC and identified adrenergic receptors agonists as a class of compounds that reduce endogenous human tau. These techniques enable the use of human neurons for high-throughput screening of drugs to treat neurodegenerative disease.

Indexed as

Cell DifferentiationDrug DiscoveryHigh-Throughput Screening AssaysCell LineCells, CulturedCell SurvivalDrug Evaluation, PreclinicalGene ExpressionGene Expression RegulationGene OrderGenetic VectorsGlutamineHumansInduced Pluripotent Stem CellsMembrane PotentialsNeuronsGlutaminetau Proteinsadrenergic receptorAlzheimer’s diseasefrontotemporal dementiahigh-content screeninghuman induced pluripotent stem cellshuman neuronsneurodegenerationneurogenin 2tauTau-lowering

Identifiers

PMID28966121
PMCPMC5639430
OpenAlexW2760524820

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.