ReviewGenes2016
The Future is The Past: Methylation QTLs in Schizophrenia.
Review in Genes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 27 citations in OpenAlex.
- Genetic risk of osteoarthritis operates during human skeletogenesis.Human molecular genetics · 2023Article
- Cross-Ancestry DNA Methylation Marks of Insulin Resistance in Pregnancy: An Integrative Epigenome-Wide Association Study.Diabetes · 2023Article
- Article
- Detecting methylation quantitative trait loci using a methylation random field method.Briefings in bioinformatics · 2021Article
- Developments in Biological Mechanisms and Treatments for Negative Symptoms and Cognitive Dysfunction of Schizophrenia.Neuroscience bulletin · 2021Review
- Genome-wide sequencing-based identification of methylation quantitative trait loci and their role in schizophrenia risk.Nature communications · 2021Article
- Beyond the looking glass: recent advances in understanding the impact of environmental exposures on neuropsychiatric disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Review
- Review
- Multi-omics integrative analysis identified SNP-methylation-mRNA: Interaction in peripheral blood mononuclear cells.Journal of cellular and molecular medicine · 2019Article
- The Translational Potential of Neuroimaging Genomic Analyses To Diagnosis And Treatment In The Mental Disorders.Proceedings of the IEEE. Institute of Electrical and Electronics Engineers · 2019Article
- Chromatin Remodeling Complex NuRD in Neurodevelopment and Neurodevelopmental Disorders.Frontiers in genetics · 2019Review
- Treating the "E" in "G × E": Trauma-Informed Approaches and Psychological Therapy Interventions in Psychosis.Frontiers in psychiatry · 2019Review
- Moderating effect of mode of delivery on the genetics of intelligence: Explorative genome-wide analyses in ALSPAC.Brain and behavior · 2018Article
- A Perspective of the Cross-Tissue Interplay of Genetics, Epigenetics, and Transcriptomics, and Their Relation to Brain Based Phenotypes in Schizophrenia.Frontiers in genetics · 2018Review
- Protocol for the EMPHASIS study; epigenetic mechanisms linking maternal pre-conceptional nutrition and children's health in India and Sub-Saharan Africa.BMC nutrition · 2017Article
- Variability of DNA Methylation within Schizophrenia Risk Loci across Subregions of Human Hippocampus.Genes · 2017Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWAS) have remarkably advanced insight into the genetic basis of schizophrenia (SCZ). Still, most of the functional variance in disease risk remains unexplained. Hence, there is a growing need to map genetic variability-to-genes-to-functions for understanding the pathophysiology of SCZ and the development of better treatments. Genetic variation can regulate various cellular functions including DNA methylation, an epigenetic mark with important roles in transcription and the mediation of environmental influences. Methylation quantitative trait loci (meQTLs) are derived by mapping levels of DNA methylation in genetically different, genotyped individuals and define loci at which DNA methylation is influenced by genetic variation. Recent evidence points to an abundance of meQTLs in brain tissues whose functional contributions to development and mental diseases are still poorly understood. Interestingly, fetal meQTLs reside in regulatory domains affecting methylome reconfiguration during early brain development and are enriched in loci identified by GWAS for SCZ. Moreover, fetal meQTLs are preserved in the adult brain and could trace early epigenomic deregulation during vulnerable periods. Overall, these findings highlight the role of fetal meQTLs in the genetic risk for and in the possible neurodevelopmental origin of SCZ.
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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.