ReviewBrain research bulletin2010
Genome-wide approaches to schizophrenia.
Review in Brain research bulletin, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 3 of them syntheses that pooled it.
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
32 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Pooled it
- Genome-wide association analysis of self-reported daytime sleepiness identifies 42 loci that suggest biological subtypes.Nature communications · 2019Pooled it
- BCL9 and C9orf5 are associated with negative symptoms in schizophrenia: meta-analysis of two genome-wide association studies.PloS one · 2013Pooled it
- A review of post-GWAS studies in schizophrenia.Translational psychiatry · 2025Review
- Schizophrenia in the genetic era: a review from development history, clinical features and genomic research approaches to insights of susceptibility genes.Metabolic brain disease · 2024Review
- A Polymorphism in theFrontiers in genetics · 2022Article
- Transcriptomic Data Analysis Reveals a Down-Expression ofBrain sciences · 2021Article
- Mass spectrometry identification of potential biomarker proteins in the 150-kD electrophoretic band in patients with schizophrenia.Medicine · 2018Article
- Reversal of dendritic phenotypes in 16p11.2 microduplication mouse model neurons by pharmacological targeting of a network hub.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Path from schizophrenia genomics to biology: gene regulation and perturbation in neurons derived from induced pluripotent stem cells and genome editing.Neuroscience bulletin · 2015Review
- Schizophrenia as a disorder of molecular pathways.Biological psychiatry · 2015Review
- A sequence variant in human KALRN impairs protein function and coincides with reduced cortical thickness.Nature communications · 2014Article
- Altered gene expression in the dorsolateral prefrontal cortex of individuals with schizophrenia.Molecular psychiatry · 2014Article
- Factor Analysis Demonstrates a Common Schizoidal Phenotype within Autistic and Schizotypal Tendency: Implications for Neuroscientific Studies.Frontiers in psychiatry · 2014Article
- Guided exploration of genomic risk for gray matter abnormalities in schizophrenia using parallel independent component analysis with reference.NeuroImage · 2013Article
- Cuprizone short-term exposure: astrocytic IL-6 activation and behavioral changes relevant to psychosis.Neurobiology of disease · 2013Article
- Genetics of childhood-onset schizophrenia.Child and adolescent psychiatric clinics of North America · 2013Review
- New findings in the genetics of schizophrenia.World journal of psychiatry · 2013Article
- An Integrative Bayesian Modeling Approach to Imaging Genetics.Journal of the American Statistical Association · 2013Article
- Maternal perspectives on the return of genetic results: context matters.American journal of medical genetics. Part A · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Schizophrenia (SZ) is a common and severe psychiatric disorder with both environmental and genetic risk factors, and a high heritability. After over 20 years of molecular genetics research, new molecular strategies, primarily genome-wide association studies (GWAS), have generated major tangible progress. This new data provides evidence for: (1) a number of chromosomal regions with common polymorphisms showing genome-wide association with SZ (the major histocompatibility complex, MHC, region at 6p22-p21; 18q21.2; and 2q32.1). The associated alleles present small odds ratios (the odds of a risk variant being present in cases vs. controls) and suggest causative involvement of gene regulatory mechanisms in SZ. (2) Polygenic inheritance. (3) Involvement of rare (<1%) and large (>100kb) copy number variants (CNVs). (4) A genetic overlap of SZ with autism and with bipolar disorder (BP) challenging the classical clinical classifications. Most new SZ findings (chromosomal regions and genes) have generated new biological leads. These new findings, however, still need to be translated into a better understanding of the underlying biology and into causal mechanisms. Furthermore, a considerable amount of heritability still remains unexplained (missing heritability). Deep resequencing for rare variants and system biology approaches (e.g., integrating DNA sequence and functional data) are expected to further improve our understanding of the genetic architecture of SZ and its underlying biology.
Indexed as
Identifiers
What 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.