Evidence map›Paper›PMID 24055772›Full record

ArticleNeurobiology of disease2014

Efficient derivation of cortical glutamatergic neurons from human pluripotent stem cells: a model system to study neurotoxicity in Alzheimer's disease.

Tandis Vazin, K Aurelia Ball, Hui Lu, Hyungju Park, Yasaman Ataeijannati, Teresa Head-Gordon, Mu-ming Poo, David V Schaffer

Erratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 92 citations in OpenAlex.

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  17. Modeling Neurodegenerative Diseases UsingFrontiers in bioengineering and biotechnology · 2022
    Review
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Tandis VazinThe Department of Chemical and Biomolecular Engineering, USA; The Department of Bioengineering, USA; Helen Wills Neuroscience Institute, USA; University of California, Berkeley, CA 94720, USA.
K Aurelia BallGraduate Group in Biophysics, USA; University of California, Berkeley, CA 94720, USA.
Hui LuHelen Wills Neuroscience Institute, USA; Division of Neurobiology, Department of Molecular and Cell Biology, USA; University of California, Berkeley, CA 94720, USA.
Hyungju ParkHelen Wills Neuroscience Institute, USA; Division of Neurobiology, Department of Molecular and Cell Biology, USA; University of California, Berkeley, CA 94720, USA.
Yasaman AtaeijannatiDepartment of Molecular and Cell Biology, USA; University of California, Berkeley, CA 94720, USA.
Teresa Head-GordonThe Department of Chemical and Biomolecular Engineering, USA; The Department of Bioengineering, USA; Graduate Group in Biophysics, USA; Department of Chemistry, USA; University of California, Berkeley, CA 94720, USA.
Mu-ming PooHelen Wills Neuroscience Institute, USA; Division of Neurobiology, Department of Molecular and Cell Biology, USA; University of California, Berkeley, CA 94720, USA.
David V SchafferThe Department of Chemical and Biomolecular Engineering, USA; The Department of Bioengineering, USA; Helen Wills Neuroscience Institute, USA; University of California, Berkeley, CA 94720, USA. Electronic address: schaffer@berkeley.edu.
University of California, Berkeley · USDivision of Chemistry · US

Funding

MOLECULAR BIOPHYSICS TRAINING GRANTT32GM008295 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI HURLEY, JAMES H, WEMMER, DAVID E · 1989 to 2022
$8.1M
NIGMS NIH HHS T32 GM008295
6 · The paper itself

Abstract

Alzheimer's disease (AD) is among the most prevalent forms of dementia affecting the aging population, and pharmacological therapies to date have not been successful in preventing disease progression. Future therapeutic efforts may benefit from the development of models that enable basic investigation of early disease pathology. In particular, disease-relevant models based on human pluripotent stem cells (hPSCs) may be promising approaches to assess the impact of neurotoxic agents in AD on specific neuronal populations and thereby facilitate the development of novel interventions to avert early disease mechanisms. We implemented an efficient paradigm to convert hPSCs into enriched populations of cortical glutamatergic neurons emerging from dorsal forebrain neural progenitors, aided by modulating Sonic hedgehog (Shh) signaling. Since AD is generally known to be toxic to glutamatergic circuits, we exposed glutamatergic neurons derived from hESCs to an oligomeric pre-fibrillar forms of Aβ known as "globulomers", which have shown strong correlation with the level of cognitive deficits in AD. Administration of such Aβ oligomers yielded signs of the disease, including cell culture age-dependent binding of Aβ and cell death in the glutamatergic populations. Furthermore, consistent with previous findings in postmortem human AD brain, Aβ-induced toxicity was selective for glutamatergic rather than GABAeric neurons present in our cultures. This in vitro model of cortical glutamatergic neurons thus offers a system for future mechanistic investigation and therapeutic development for AD pathology using human cell types specifically affected by this disease.

Indexed as

Age FactorsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCell DeathCells, CulturedCerebral CortexFemaleGABAergic NeuronsGlutamic AcidHedgehog ProteinsHumansNeuronsPluripotent Stem CellsRats, Inbred F344Amyloid beta-PeptidesGlutamic AcidHedgehog ProteinsAlzheimer's diseaseAmyloid betaCorticalGlutamatergicHumanIn vitro modelNeuronPluripotentStem cell

Identifiers

PMID24055772
PMCPMC4122237
OpenAlexW2052147188

What OpenQuestion holds

Textmetadata
LicenceTDM
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.