Evidence map›Paper›PMID 36764297›Full record

ArticleStem cell reports2023

BMP4-SMAD1/5/9-RUNX2 pathway activation inhibits neurogenesis and oligodendrogenesis in Alzheimer's patients' iPSCs in senescence-related conditions.

Daiki Nakatsu, Rina Kunishige, Yuki Taguchi, Naeko Shinozaki-Narikawa, Kishiko Osaka, Kayo Yokomizo, Mami Ishida, Shunsuke Takei, Shoko Yamasaki, Keita Hagiya and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2023. 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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Integrative multi-omics approaches identify molecular pathways and improve Alzheimer's disease risk prediction.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Repurposing medications to prevent psychosis.Npj mental health research · 2025
    Review
  4. Review
  5. Article
  6. Crosstalk between bone and brain in Alzheimer's disease: Mechanisms, applications, and perspectives.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Review
  7. Article
  8. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Daiki NakatsuCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan.
Rina KunishigeCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan; Multimodal Cell Analysis Collaborative Research Cluster, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan.
Yuki TaguchiCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan; Multimodal Cell Analysis Collaborative Research Cluster, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan.
Naeko Shinozaki-NarikawaCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan.
Kishiko OsakaCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan.
Kayo YokomizoCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan.
Mami IshidaCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan.
Shunsuke TakeiSystem Development Department, Technology Solutions Sector, Healthcare Business Unit, Nikon Corporation, 471, Nagaodai-cho, Sakae-ku, Yokohama, Kanagawa 244-8533, Japan.
Shoko YamasakiMathematical Sciences Research Laboratory, Research & Development Division, Nikon Corporation, 471, Nagaodai-cho, Sakae-ku, Yokohama, Kanagawa 244-8533, Japan.
Keita HagiyaFujifilm Corporation, 7-3 Akasaka 9, Minato-ku, Tokyo 107-0052, Japan.
Kotaro HattoriDepartment of Bioresources, Medical Genome Center, National Center of Neurology and Psychiatry, 4-1-1, Ogawahigashi-cho, Kodaira, Tokyo 187-8551, Japan.
Tadashi TsukamotoDepartment of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1, Ogawahigashi-cho, Kodaira, Tokyo 187-8551, Japan.
Masayuki MurataCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan; Multimodal Cell Analysis Collaborative Research Cluster, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan.
Fumi KanoCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa 226-8503, Japan. Electronic address: kano.f.aa@m.titech.ac.jp.
Tokyo Institute of Technology · JPNational Center of Neurology and Psychiatry · JPNikon (Japan) · JPFujifilm (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to increasing β-amyloid plaque deposition and tau tangle formation, inhibition of neurogenesis has recently been observed in Alzheimer's disease (AD). This study generated a cellular model that recapitulated neurogenesis defects observed in patients with AD, using induced pluripotent stem cell lines derived from sporadic and familial AD (AD iPSCs). AD iPSCs exhibited impaired neuron and oligodendrocyte generation when expression of several senescence markers was induced. Compound screening using these cellular models identified three drugs able to restore neurogenesis, and extensive morphological quantification revealed cell-line- and drug-type-dependent neuronal generation. We also found involvement of elevated Sma- and Mad-related protein 1/5/9 (SMAD1/5/9) phosphorylation and greater Runt-related transcription factor 2 (RUNX2) expression in neurogenesis defects in AD. Moreover, BMP4 was elevated in AD iPSC medium during neural differentiation and cerebrospinal fluid of patients with AD, suggesting a BMP4-SMAD1/5/9-RUNX2 signaling pathway contribution to neurogenesis defects in AD under senescence-related conditions.

Indexed as

Alzheimer DiseaseInduced Pluripotent Stem CellsAmyloid beta-PeptidesBone Morphogenetic Protein 4Core Binding Factor Alpha 1 SubunitHumansNeurogenesisNeuronsSmad ProteinsAmyloid beta-PeptidesBMP4 protein, humanBone Morphogenetic Protein 4Core Binding Factor Alpha 1 SubunitRUNX2 protein, humanSmad ProteinsAlzheimer’s diseaseBMP4compound screeninginduced pluripotent stem cell (iPSC)morphological analysisneurogenesisRUNX2SMAD1/5/9

Identifiers

PMID36764297
PMCPMC10031282
OpenAlexW4319728569

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.