Evidence map›Paper›PMID 40775243›Full record

ArticleSchizophrenia (Heidelberg, Germany)2025

The association between plasma betaine level and brain structural changes in schizophrenia.

Favour Omileke, Tempei Ikegame, Shimon Tonsho, Shunsuke Mori, Eimu Shoji, Masahiro Kiyota, Takuto Minami, Eureka Kumagai, Tatsuro Asai, Kenji Kirihara and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Schizophrenia (Heidelberg, Germany), 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. 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

16 authors.

Favour OmilekeDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tempei IkegameDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Shimon TonshoDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Shunsuke MoriDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Eimu ShojiDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masahiro KiyotaDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Takuto MinamiDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0009-0008-5667-0173
Eureka KumagaiDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tatsuro AsaiDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kenji KiriharaDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-9703-9133
Shinsuke KoikeCenter for Evolutionary Cognitive Sciences, Graduate School of Art and Sciences, The University of Tokyo, Tokyo, Japan.
Seiichiro JindeDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kouhei KamiyaDepartment of Radiology, Toho University Omori Medical Center, Tokyo, Japan.
Osamu AbeDepartment of Radiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-1180-2629
Kiyoto KasaiDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-4443-4535
Naohiro OkadaDepartment of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. nokada-tky@g.ecc.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0002-8338-2758

Funding

Japan Agency for Medical Research and Development (AMED) JP18dm0307001Japan Agency for Medical Research and Development (AMED) JP18dm0307004Japan Agency for Medical Research and Development (AMED) JP19dm0207069Japan Agency for Medical Research and Development (AMED) JP23wm0625001MEXT | Japan Science and Technology Agency (JST) JPMJMS2021MEXT | Japan Society for the Promotion of Science (JSPS) JP18K15478MEXT | Japan Society for the Promotion of Science (JSPS) JP21H05171MEXT | Japan Society for the Promotion of Science (JSPS) JP21H05174MEXT | Japan Society for the Promotion of Science (JSPS) JP22H04926MEXT | Japan Society for the Promotion of Science (JSPS) JP22K18419
6 · The paper itself

Abstract

Previous studies on metabolic profiling have shown decreased plasma levels of betaine in schizophrenia. Betaine serves as a substrate of betaine-homocysteine methyltransferase, which converts homocysteine to methionine. A decrease in betaine may lead to the elevation of homocysteine and an insufficient supply of methyl donors, which may affect DNA methylation. To explore how decreased betaine levels could affect brain structural changes often observed in schizophrenia, the present study investigated the relationships in 27 patients with chronic schizophrenia and 49 healthy comparison individuals. We found that the effects of betaine on brain volume are group-specific, and significant correlations between betaine and notable brain areas implicated in schizophrenia's pathophysiology including the superior temporal gyrus. These findings suggest that betaine levels may contribute to aberrant structural changes in schizophrenia.

Identifiers

PMID40775243
PMCPMC12332064

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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.