ArticleMolecular neurobiology2025
From Clinic to Mechanisms: Multi-Omics Provide New Insights into Cerebrospinal Fluid Metabolites and the Spectrum of Psychiatric Disorders.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Diagnosing autoimmune encephalitis in psychiatry: clinical recommendations and unresolved challenges from the GENERATE network.Molecular psychiatry · 2026Review
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
Cerebrospinal fluid (CSF) is crucial in maintaining brain homeostasis by facilitating waste clearance, nutrient transport, and immune signaling. However, the links between CSF metabolites and psychiatric disorders, as well as the underlying mechanisms, remain largely unexamined. We conducted a bidirectional two-sample Mendelian randomization analysis to investigate potential causal relationships between CSF metabolites and 12 psychiatric disorders. Summary data for psychiatric disorders were sourced from the Psychiatric Genomics Consortium, while information on CSF metabolites was derived from two studies within the Wisconsin Alzheimer's Disease cohort. Causal estimates and pleiotropy were assessed using several robust methods, including inverse-variance-weighted (IVW) analysis, weighted median analysis, MR-Egger regression, and the MR-Egger test. Furthermore, a transcriptome-wide association study was conducted to explore potential mechanisms and shared etiologies between CSF metabolites and psychiatric disorders. The genetic risk of eating disorders (ED) can be increased by leucine (OR = 1.55, 95% CI: 1.21-1.97, P = 4.35 × 10⁻
Indexed as
Identifiers
40085352What Socratic 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 Socratic graph.