SynthesisPsychiatric genetics2012
Microduplications disrupting the MYT1L gene (2p25.3) are associated with schizophrenia.
Synthesis in Psychiatric genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 50 citations in OpenAlex.
- MYT1L: A systematic review of genetic variation encompassing schizophrenia and autism.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2020Pooled it
- Childhood-Onset Schizophrenia: A Systematic Overview of Its Genetic Heterogeneity From Classical Studies to the Genomic Era.Frontiers in genetics · 2019Pooled it
- Distribution of disease-associated copy number variants across distinct disorders of cognitive development.Journal of the American Academy of Child and Adolescent Psychiatry · 2013Pooled it
- A Novel Variant in the MYT1L Gene Shared by Three Individuals with Neuropsychiatric and Neurodevelopmental Manifestations in a Family.Indian journal of psychological medicine · 2026Article
- Autism- and intellectual disability-associated MYT1L mutation alters human cortical interneuron differentiation, maturation, and physiology.Stem cell reports · 2025Article
- Article
- 2p25.3 microduplications involving MYT1L: further phenotypic characterization through an assessment of 16 new cases and a literature review.European journal of human genetics : EJHG · 2023Review
- MYT1L haploinsufficiency in human neurons and mice causes autism-associated phenotypes that can be reversed by genetic and pharmacologic intervention.Molecular psychiatry · 2023Article
- The genetic basis of onset age in schizophrenia: evidence and models.Frontiers in genetics · 2023Review
- Myt1l haploinsufficiency leads to obesity and multifaceted behavioral alterations in mice.Molecular autism · 2022Article
- Circulating microRNA sequencing revealed miRNome patterns in hematology and oncology patients aiding the prognosis of invasive aspergillosis.Scientific reports · 2022Article
- Long non-coding RNA Neat1 regulates adaptive behavioural response to stress in mice.Translational psychiatry · 2020Article
- A Link between Genetic Disorders and Cellular Impairment, Using Human Induced Pluripotent Stem Cells to Reveal the Functional Consequences of Copy Number Variations in the Central Nervous System-A Close Look at Chromosome 15.International journal of molecular sciences · 2020Review
- Perinatal administration of phencyclidine alters expression of Lingo-1 signaling pathway proteins in the prefrontal cortex of juvenile and adult rats.Neuronal signaling · 2018Article
- Myt1L Promotes Differentiation of Oligodendrocyte Precursor Cells and is Necessary for Remyelination After Lysolecithin-Induced Demyelination.Neuroscience bulletin · 2018Article
- Systems genetics analysis of pharmacogenomics variation during antidepressant treatment.The pharmacogenomics journal · 2018Article
- Associations of the Intellectual Disability Gene MYT1L with Helix-Loop-Helix Gene Expression, Hippocampus Volume and Hippocampus Activation During Memory Retrieval.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- Article
- Modulating Neuroinflammation to Treat Neuropsychiatric Disorders.BioMed research international · 2017Review
- Epigenetic Basis of Mental Illness.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Childhood-onset schizophrenia (COS) is a rare severe form of schizophrenia that may have greater salient genetic risk. Despite evidence for high heritability, conclusive genetic causes of schizophrenia remain elusive. Recent genomic technologies in concert with large case-control cohorts have led to several associations of highly penetrant rare copy number variants (CNVs) and schizophrenia. We previously reported two patients with COS who carried a microduplication disrupting the PXDN and MYT1L genes at 2p25.3. This rate of duplications within our COS population (N=92) is significantly higher than that in 2026 healthy controls (P=0.002). As a replication, we report a meta-analysis of four recently published studies that together provide strong evidence for an association between variably sized microduplications involving the MYT1L gene and schizophrenia. None have reported this separately. Altogether, among 5325 patients and 9279 controls, 10 microduplications were observed: nine in patients and one in a control (odds ratio=15.7, P=0.001). Further, the 2% rate observed in our COS patients is also significantly higher than the rate in adult-onset cases (0.14%, odds ratio=16.6, P=0.01). This report adds to the growing body of literature implicating rare CNVs as risk factors for schizophrenia and shows that some risk CNVs are more common among extreme early-onset cases.
Indexed as
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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.