Evidence map›Paper›PMID 40541177›Full record

ArticleStem cell reports2025

BMP, MEK, and WNT inhibition with NGN2 expression for rapid generation of hiPSC-derived neurons amenable to regional patterning.

Carina Habich, Alexandra Kowalski, Astrid Wachter, Michaela J Heimann, Michael Wolf, Markus P Kummer, Nathalie Nicolaisen, Christopher Sliwinski, Lydia Reinhardt, Veronika Heil and 18 more

Abstract read
In one paragraph

Article in Stem cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

28 authors.

Carina HabichAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Alexandra KowalskiInstitute of Molecular and Cell Biology, Mannheim University of Applied Sciences, 68163 Mannheim, Germany.
Astrid WachterAbbVie Deutschland GmbH & Co. KG, Genomics Research Center, Knollstrasse, 67061 Ludwigshafen, Germany.
Michaela J HeimannAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Michael WolfAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Markus P KummerAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Nathalie NicolaisenAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Christopher SliwinskiAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Lydia ReinhardtAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Veronika HeilAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Timo LangeAbbVie Deutschland GmbH & Co. KG, Genomics Research Center, Knollstrasse, 67061 Ludwigshafen, Germany.
Christopher UntuchtAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Loan N MillerAbbVie Inc., Pharmacology and Pathology, Lake County, IL 60064, USA.
Jürgen KorffmannAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Daniela GeistAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
David SchöndorfAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Heyne LeeAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Lamiaa BahnassawyAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Benjamin Mielich-SüssAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Melanie S BrennanAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Ruven WilkensAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Julian RöweAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Ian WeidlingAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Rüdiger RudolfInstitute of Molecular and Cell Biology, Mannheim, University of Applied Sciences, D-68163 Mannheim, Germany, and Interdisciplinary Center for Neurosciences, Heidelberg, University, 69117 Heidelberg, Germany; Center for Mass Spectrometry and Optical Spectroscopy, Mannheim University of Applied Sciences, 68163 Mannheim, Germany.
Mathias HafnerInstitute of Molecular and Cell Biology, Mannheim, University of Applied Sciences, D-68163 Mannheim, Germany, and Interdisciplinary Center for Neurosciences, Heidelberg, University, 69117 Heidelberg, Germany; Institute of Medical Technology, Heidelberg University and Mannheim University of Applied Sciences, 69117 Heidelberg, Germany.
Justine D ManosAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Miroslav CikAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany.
Peter ReinhardtAbbVie Deutschland GmbH & Co. KG, Neuroscience Discovery, Knollstrasse, 67061 Ludwigshafen, Germany. Electronic address: peter.reinhardt@abbvie.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human induced pluripotent stem cells (hiPSCs) are a promising tool for studying neurological diseases and developing therapies for neurodegenerative diseases. Differentiation of hiPSCs into neurons can be achieved by dual SMAD inhibition (dSMADi) or by induced neurogenin 2 (NGN2) overexpression ("iNGN2"). Starting directly from hiPSCs, iNGN2 shortens the time to a neuronal stage but leads to neurons partially resembling peripheral or posterior fates while dSMADi more faithfully recapitulates telencephalic development. To modify the iNGN2 approach, we applied an accelerated induction paradigm that is dependent on the inhibition of BMP, MEK, and WNT pathways ("BMWi"), to commit hiPSCs into a telencephalic fate before iNGN2. The resulting neurons showed strong expression of telencephalic markers, with decreased levels of peripheral and posterior marker genes compared to iNGN2 alone. The resulting telencephalic neurons are suitable for a tau aggregation assay. Furthermore, we could demonstrate that during BMWi treatment, the cells are amenable to additional regional patterning cues. This allowed the generation of neurons from different regions of the CNS and peripheral nervous system (PNS), which will significantly facilitate in vitro modeling of a range of neurodevelopmental and neurodegenerative disorders.

Indexed as

Basic Helix-Loop-Helix ProteinsBody PatterningBone Morphogenetic ProteinsInduced Pluripotent Stem CellsMitogen-Activated Protein Kinase KinasesNerve Tissue ProteinsNeuronsCell DifferentiationHumansWnt Signaling PathwayBasic Helix-Loop-Helix ProteinsBone Morphogenetic ProteinsMitogen-Activated Protein Kinase KinasesNerve Tissue ProteinsNEUROG2 protein, humanAlzheimer's diseasecortical neuronsdisease modelingdopaminergic neuronshuman induced pluripotent stem cellsmotoneuronsneural developmentneurodegenerative diseasesParkinson's disease

Identifiers

PMID40541177
PMCPMC12277818

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.