Evidence map›Paper›PMID 32732995›Full record

ArticleCommunications biology2020

Metabolomic and transcriptomic signatures of prenatal excessive methionine support nature rather than nurture in schizophrenia pathogenesis.

Siwei Chen, Wedad Alhassen, Ryan Yoshimura, Angele De Silva, Geoffrey W Abbott, Pierre Baldi, Amal Alachkar

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  8. Rhea, the reaction knowledgebase in 2022.Nucleic acids research · 2022
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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

7 authors at 1 institution in 1 country.

Siwei Chen *Department of Computer Science, School of Information and Computer Sciences, University of California-Irvine, Irvine, CA, 92697, USA.
Wedad Alhassen *Department of Pharmaceutical Sciences, University of California-Irvine, Irvine, CA, 92697, USA.
Ryan YoshimuraDepartment of Pharmaceutical Sciences, University of California-Irvine, Irvine, CA, 92697, USA.
Angele De SilvaBioelectricity Laboratory, Department of Physiology and Biophysics, School of Medicine, University of California-Irvine, Irvine, CA, 92697, USA.ORCID http://orcid.org/0000-0002-3243-3893
Geoffrey W AbbottBioelectricity Laboratory, Department of Physiology and Biophysics, School of Medicine, University of California-Irvine, Irvine, CA, 92697, USA.
Pierre BaldiDepartment of Computer Science, School of Information and Computer Sciences, University of California-Irvine, Irvine, CA, 92697, USA.
Amal AlachkarInstitute for Genomics and Bioinformatics, School of Information and Computer Sciences, University of California-Irvine, Irvine, CA, 92697, USA. aalachka@uci.edu.ORCID http://orcid.org/0000-0002-5365-1726
University of California, Irvine · US

Funding

Ion Channel Transporter InteractionsR35GM130377 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Geoffrey W Abbott · 2019 to 2026
$4.0M
Bioinformatics Tools for Circadian BiologyR01GM123558 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Pierre Baldi · 2017 to 2026
$2.4M
NIGMS NIH HHS R01 GM123558NIGMS NIH HHS R35 GM130377
6 · The paper itself

Abstract

The imbalance of prenatal micronutrients may perturb one-carbon (C1) metabolism and increase the risk for neuropsychiatric disorders. Prenatal excessive methionine (MET) produces in mice behavioral phenotypes reminiscent of human schizophrenia. Whether in-utero programming or early life caregiving mediate these effects is, however, unknown. Here, we show that the behavioral deficits of MET are independent of the early life mother-infant interaction. We also show that MET produces in early life profound changes in the brain C1 pathway components as well as glutamate transmission, mitochondrial function, and lipid metabolism. Bioinformatics analysis integrating metabolomics and transcriptomic data reveal dysregulations of glutamate transmission and lipid metabolism, and identify perturbed pathways of methylation and redox reactions. Our transcriptomics Linkage analysis of MET mice and schizophrenia subjects reveals master genes involved in inflammation and myelination. Finally, we identify potential metabolites as early biomarkers for neurodevelopmental defects and suggest therapeutic targets for schizophrenia.

Indexed as

AnimalsBiomarkersBrainDisease Models, AnimalFemaleHumansMetabolomeMetabolomicsMethionineMicePregnancyPrenatal Nutritional Physiological PhenomenaSchizophreniaTranscriptomeBiomarkersMethionine

Identifiers

PMID32732995
PMCPMC7393105
OpenAlexW3045967457

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.