ArticleMolecular neurobiology2025
Identification of Mood Disorders Causal Genes by Integrating the Brain Proteome and Transcriptome.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Genome-wide association analysis studies (GWAS) have revealed loci associated with mood disorders (MD). However, the mechanism of action of these loci on drug targets for MD remains uncertain. Therefore, in this study, our aim was to identify causal genes for MD by integrating brain transcriptomic and proteomic expression data. We employed a combination of PWAS (proteome-wide association study), TWAS (transcriptome-wide association study), Mendelian randomization (MR), Bayesian colocalization analysis, as well as conditional and joint analysis to identify causal genes for MD in the brain. To validate our findings, we also utilized the GEO dataset. Our comprehensive analyses indicated that GPX1 and GMPPB were the most promising target genes, as they exhibited the highest causal association with MD. GPX1 exhibited the highest causal association index with MD, followed by GMPPB. Increased abundance of these two genes was associated with an elevated risk of developing MD, and both were predominantly expressed in the cerebral cortex.
Indexed as
Identifiers
40025292What OpenQuestion holds
Registered trials
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.