Publication date: Oct 01, 2026
Genome-wide association studies (GWAS) have revolutionized our understanding of the genetic architecture of psychiatric disorders. However, the interpretation of these findings remains challenging, as most risk loci reside in non-coding regions, obscuring the underlying molecular mechanisms. To elucidate the functional consequences of psychiatric risk variants, we implemented a multi-omics Bayesian colocalization framework using transcript, protein and metabolite levels for attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder (BIP), major depressive disorder (MDD), and schizophrenia (SCZ). Sixty-five SCZ, BIP, and MDD GWAS signals colocalized with immune cell-type-specific expression quantitative trait loci (eQTL), targeting 70 genes. Notably, they included 17 histone-encoding genes colocalized from five GWAS signals. These signals subsequently colocalized with protein QTL (pQTL), targeting 310 proteins enriched in various immune-related pathways (P
Semantics
| Type | Source | Name |
|---|---|---|
| disease | MESH | psychiatric disorder |
| disease | MESH | autism spectrum disorder |
| disease | MESH | bipolar disorder |
| disease | MESH | major depressive disorder |
| disease | MESH | schizophrenia |
| disease | MESH | included |
| disease | MESH | Attention Deficit Disorder with Hyperactivity |
| disease | MESH | Genetic Predisposition to Disease |