Evidence map›Paper›PMID 39211392›Full record

ArticleFrontiers in cell and developmental biology2024

Establishment of a novel amyotrophic lateral sclerosis patient (

Kinya Matsuo, Jun Nagamatsu, Kazuhiro Nagata, Ryusei Umeda, Takaya Shiota, Satoru Morimoto, Naoki Suzuki, Masashi Aoki, Hideyuki Okano, Masayuki Nakamori and 1 more

Abstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
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

11 authors.

Kinya MatsuoDepartment of Neurology and Clinical Neuroscience, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan.
Jun NagamatsuYamaguchi University Graduate School of Medicine, Yamaguchi, Japan.
Kazuhiro NagataYamaguchi University Graduate School of Medicine, Yamaguchi, Japan.
Ryusei UmedaYamaguchi University Graduate School of Medicine, Yamaguchi, Japan.
Takaya ShiotaYamaguchi University Graduate School of Medicine, Yamaguchi, Japan.
Satoru MorimotoKeio University, Regenerative Medicine Research Center, Kawasaki, Kanagawa, Japan.
Naoki SuzukiDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Masashi AokiDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Hideyuki OkanoKeio University, Regenerative Medicine Research Center, Kawasaki, Kanagawa, Japan.
Masayuki NakamoriDepartment of Neurology and Clinical Neuroscience, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan.
Hideaki NishiharaDepartment of Neurology and Clinical Neuroscience, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a major neurodegenerative disease for which there is currently no curative treatment. The blood-brain barrier (BBB), multiple physiological functions formed by mainly specialized brain microvascular endothelial cells (BMECs), serves as a gatekeeper to protect the central nervous system (CNS) from harmful molecules in the blood and aberrant immune cell infiltration. The accumulation of evidence indicating that alterations in the peripheral milieu can contribute to neurodegeneration within the CNS suggests that the BBB may be a previously overlooked factor in the pathogenesis of ALS. Animal models suggest BBB breakdown may precede neurodegeneration and link BBB alteration to the disease progression or even onset. However, the lack of a useful patient-derived model hampers understanding the pathomechanisms of BBB dysfunction and the development of BBB-targeted therapies. In this study, we differentiated BMEC-like cells from human induced pluripotent stem cells (hiPSCs) derived from ALS patients to investigate BMEC functions in ALS patients.

Indexed as

amyotrophic lateral sclerosisblood-brain barrierhuman induced pluripotent stem cellsTDP-43Wnt/β-catenin signaling

Identifiers

PMID39211392
PMCPMC11357944

What OpenQuestion holds

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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.