ArticleMolecular psychiatry2023
Psychiatric disorders and brain white matter exhibit genetic overlap implicating developmental and neural cell biology.
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Exploration of Genetic Overlap of Brain Phenotypes With Schizophrenia: Different Methods Provide Complementary Insights.Schizophrenia bulletin · 2026Article
- Shared genetic architecture between ADHD and intelligence varies across ADHD subtypes.BMC medicine · 2026Article
- Hemispheric Asymmetry in the Genetic Overlap between Schizophrenia and White Matter Microstructure.Cyborg and bionic systems (Washington, D.C.) · 2026Article
- Bivariate GSA-MiXeR: A Novel Tool for Functional Genomic Analyses Implicates Diverse Neural Cell Types for Psychiatric and Neurodegenerative Disorders.medRxiv : the preprint server for health sciences · 2025Article
- Age-related differences in axon pruning and myelination may alter neural signaling in autism spectrum disorder.Molecular autism · 2025Article
- The relationship between vitamin D levels and depression: a genetically informed study.Nutrition journal · 2025Article
- Brain Tumors, AI and Psychiatry: Predicting Tumor-Associated Psychiatric Syndromes with Machine Learning and Biomarkers.International journal of molecular sciences · 2025Review
- Mapping Structural Neuroimaging Trajectories in Bipolar Disorder: Neurobiological and Clinical Implications.Biological psychiatry · 2025Review
- Genome-wide analysis identifies novel shared loci between depression and white matter microstructure.Molecular psychiatry · 2025Article
- Cortical myelin mapping in antipsychotic medication-naïve, first-episode psychosis patients.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Parkinsonism, Psychomotor Slowing, Negative and Depressive Symptoms in Schizophrenia Spectrum and Mood Disorders: Exploring Their Intricate Nexus Using a Network Analytic Approach.Schizophrenia bulletin · 2025Article
- Genome-wide Pleiotropy Analysis Reveals Shared Genetic Associations between Type 2 Diabetes Mellitus and Subcortical Brain Volumes.Research (Washington, D.C.) · 2025Article
- Deriving Mendelian Randomization-based Causal Networks of Brain Imaging Phenotypes and Bipolar Disorder.medRxiv : the preprint server for health sciences · 2024Article
- Investigating the shared genetic architecture between depression and subcortical volumes.Nature communications · 2024Article
- Glymphatic function assessment with diffusion tensor imaging along the perivascular space in patients with major depressive disorder and its relation to cerebral white-matter alteration.Quantitative imaging in medicine and surgery · 2024Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Improved understanding of the shared genetic architecture between psychiatric disorders and brain white matter may provide mechanistic insights for observed phenotypic associations. Our objective is to characterize the shared genetic architecture of bipolar disorder (BD), major depression (MD), and schizophrenia (SZ) with white matter fractional anisotropy (FA) and identify shared genetic loci to uncover biological underpinnings. We used genome-wide association study (GWAS) summary statistics for BD (n = 413,466), MD (n = 420,359), SZ (n = 320,404), and white matter FA (n = 33,292) to uncover the genetic architecture (i.e., polygenicity and discoverability) of each phenotype and their genetic overlap (i.e., genetic correlations, overlapping trait-influencing variants, and shared loci). This revealed that BD, MD, and SZ are at least 7-times more polygenic and less genetically discoverable than average FA. Even in the presence of weak genetic correlations (range = -0.05 to -0.09), average FA shared an estimated 42.5%, 43.0%, and 90.7% of trait-influencing variants as well as 12, 4, and 28 shared loci with BD, MD, and SZ, respectively. Shared variants were mapped to genes and tested for enrichment among gene-sets which implicated neurodevelopmental expression, neural cell types, myelin, and cell adhesion molecules. For BD and SZ, case vs control tract-level differences in FA associated with genetic correlations between those same tracts and the respective disorder (r
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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 Socratic graph.