ArticleSchizophrenia bulletin2023
Shared Genetic Loci Between Schizophrenia and White Blood Cell Counts Suggest Genetically Determined Systemic Immune Abnormalities.
Article in Schizophrenia bulletin, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed, 30 citations in OpenAlex.
- Disorder-specific and shared genetic architecture underlying schizophrenia and bipolar disorder.medRxiv : the preprint server for health sciences · 2026Article
- Neuroinflammation: an unfortunate term to describe schizophrenia.Molecular psychiatry · 2026Review
- Dissecting the genetic relationship between severe mental disorders and autoimmune diseases.Brain, behavior, and immunity · 2026Article
- Shared genetic architecture between schizophrenia and gastrointestinal diseases: insights from large-scale genome-wide cross-trait analysis.Annals of general psychiatry · 2026Article
- B cell pathways implicate shared genetic architecture between schizophrenia and immune-mediated diseases.Journal of translational medicine · 2026Article
- Using Multi-Omic Signatures in the Understanding of Inflammation and Psychosis: Can Methylation-Derived White Blood Cell Proportions Guide Early Intervention?Biological psychiatry global open science · 2025Article
- The influencing factors of cognitive dysfunction in patients after cardiac surgery and the construction of a nomogram prediction model.European journal of medical research · 2025Article
- The genetic overlap between major depressive disorder, white blood cell counts and interleukin 6.Journal of affective disorders reports · 2025Article
- Allergy-unrelated eosinophil activation in the peripheral blood of children with neurodevelopmental disorders.Frontiers in neurology · 2025Article
- Unraveling the heart-brain axis: shared genetic mechanisms in cardiovascular diseases and Schizophrenia.Schizophrenia (Heidelberg, Germany) · 2024Article
- Immunophenotypes in psychosis: is it a premature inflamm-aging disorder?Molecular psychiatry · 2024Review
- Dissecting the genetic overlap between severe mental disorders and markers of cellular aging: Identification of pleiotropic genes and druggable targets.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Immune dysregulation is associated with symptom dimensions and cognitive deficits in schizophrenia: accessible evidence from complete blood count.BMC psychiatry · 2024Article
- Association between psychiatric symptoms with multiple peripheral blood sample test: a 10-year retrospective study.Frontiers in psychiatry · 2024Article
- Hematological and inflammatory markers in Han Chinese patients with drug-free schizophrenia: relationship with symptom severity.Frontiers in immunology · 2024Article
- Neuroinflammation and schizophrenia - is there a link?Frontiers in psychiatry · 2024Article
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundImmune mechanisms are indicated in schizophrenia (SCZ). Recent genome-wide association studies (GWAS) have identified genetic variants associated with SCZ and immune-related phenotypes. Here, we use cutting edge statistical tools to identify shared genetic variants between SCZ and white blood cell (WBC) counts and further understand the role of the immune system in SCZ. STUDY
designGWAS results from SCZ (patients, n = 53 386; controls, n = 77 258) and WBC counts (n = 56 3085) were analyzed. We applied linkage disequilibrium score regression, the conditional false discovery rate method and the bivariate causal mixture model for analyses of genetic associations and overlap, and 2 sample Mendelian randomization to estimate causal effects. STUDY
resultsThe polygenicity for SCZ was 7.5 times higher than for WBC count and constituted 32%-59% of WBC count genetic loci. While there was a significant but weak positive genetic correlation between SCZ and lymphocytes (rg = 0.05), the conditional false discovery rate method identified 383 shared genetic loci (53% concordant effect directions), with shared variants encompassing all investigated WBC subtypes: lymphocytes, n = 215 (56% concordant); neutrophils, n = 158 (49% concordant); monocytes, n = 146 (47% concordant); eosinophils, n = 135 (56% concordant); and basophils, n = 64 (53% concordant). A few causal effects were suggested, but consensus was lacking across different Mendelian randomization methods. Functional analyses indicated cellular functioning and regulation of translation as overlapping mechanisms.
conclusionsOur results suggest that genetic factors involved in WBC counts are associated with the risk of SCZ, indicating a role of immune mechanisms in subgroups of SCZ with potential for stratification of patients for immune targeted treatment.
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