Evidence map›Paper›PMID 41866870›Full record

ArticleNeuropsychopharmacology reports2026

Differential Neuronal Development in iPSC-Derived Neural Stem Cells From Monozygotic Twin Cases With Treatment-Resistant Schizophrenia and Discordant Responses to Clozapine.

Shotaro Kawano, Sayaka Katayama, Masaya Ogawa, Rei Endo, Naoto Ikeda, Yuuri Ikeuchi, Tomoki Mita, Hikari Takei, Nanaka Gotoda-Nishimura, Daiki Miura and 4 more

Abstract readTwin Study
In one paragraph

Article in Neuropsychopharmacology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Shotaro KawanoLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Sayaka KatayamaLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Masaya OgawaLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Rei EndoLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Naoto IkedaLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Yuuri IkeuchiLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Tomoki MitaLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Hikari TakeiLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Nanaka Gotoda-NishimuraLaboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Japan.
Daiki MiuraLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Hotaka FukushimaLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.
Hitoshi HashimotoLaboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Japan.
Ryota HashimotoDepartment of Pathology of Mental Diseases, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Japan.
Takanobu NakazawaLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.

Funding

Japan Agency for Medical Research and Development JP19gm1310003Japan Agency for Medical Research and Development JP21dm0207117Japan Agency for Medical Research and Development JP24wn0425012Japan Agency for Medical Research and Development JP25ama121052Japan Agency for Medical Research and Development JP25ama121054Japan Agency for Medical Research and Development JP25wm0625521Japan Society for the Promotion of Science JP23H00395Japan Society for the Promotion of Science JP23KJ1953Japan Society for the Promotion of Science JP24K02182Japan Society for the Promotion of Science JP24K22022Ministry of Education, Culture, Sports, Science and Technology JP18H05416Takeda Science Foundation
6 · The paper itself

Abstract

Treatment-resistant schizophrenia (TRS) affects 20%-30% of individuals diagnosed with schizophrenia and is effectively managed with clozapine. However, the molecular and cellular mechanisms that underlie its efficacy remain largely unclear. We previously generated induced pluripotent stem cell (iPSC) lines from a unique pair of monozygotic twins with TRS. One twin responded to clozapine (CLZ-res), while the other did not (CLZ-non-res). Building on our previous study of these twins, we included healthy controls and focused on the early developmental stages of neuronal differentiation. To investigate the phenotypic differences in the developmental stages of neural cells between patient-derived cells, we differentiated each iPSC line-from both patients and healthy individuals-into neural stem cells (NSCs) and subsequently induced the differentiation of NSCs into neurons. Our results demonstrated that NSCs derived from patients' iPSC lines exhibited impaired neuronal differentiation, with a more pronounced reduction in differentiation observed in CLZ-non-res cells than in CLZ-res cells. RNA sequencing analysis revealed significant differences in the expression of genes involved in neuronal development between CLZ-res and CLZ-non-res cells. These findings suggest that the differences in neuronal development may contribute to the variability in clozapine responsiveness. Although this study is limited to a single twin pair, this unique human model provides valuable insights into the molecular and cellular mechanisms underlying differential clozapine responses, offering a promising framework for the development of effective treatments for patients with TRS.

Indexed as

Antipsychotic AgentsClozapineInduced Pluripotent Stem CellsNeural Stem CellsNeurogenesisSchizophrenia, Treatment-ResistantAdultCell DifferentiationFemaleHumansMaleNeuronsTwins, MonozygoticAntipsychotic AgentsClozapineclozapineiPSCmonozygotic twinsneural developmentneuronal differentiationtreatment‐resistant schizophrenia

Identifiers

PMID41866870
PMCPMC13283898

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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.