ReviewSchizophrenia research2016
Understanding the genetic liability to schizophrenia through the neuroepigenome.
Review in Schizophrenia research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 27 citations in OpenAlex.
- Schizophrenia-associated differential DNA methylation in brain is distributed across the genome and annotated to MAD1L1, a locus at which DNA methylation and transcription phenotypes share genetic variation with schizophrenia risk.Translational psychiatry · 2022Article
- CRISPR-based functional evaluation of schizophrenia risk variants.Schizophrenia research · 2020Article
- Molecular windows into the human brain for psychiatric disorders.Molecular psychiatry · 2019Review
- Local and global chromatin interactions are altered by large genomic deletions associated with human brain development.Nature communications · 2018Article
- The Vast Complexity of the Epigenetic Landscape during Neurodevelopment: An Open Frame to Understanding Brain Function.International journal of molecular sciences · 2018Review
- N-3 (Omega-3) Fatty Acids: Effects on Brain Dopamine Systems and Potential Role in the Etiology and Treatment of Neuropsychiatric Disorders.CNS & neurological disorders drug targets · 2018Review
- Open chromatin profiling of human postmortem brain infers functional roles for non-coding schizophrenia loci.Human molecular genetics · 2017Article
- Rethinking the Epigenetic Framework to Unravel the Molecular Pathology of Schizophrenia.International journal of molecular sciences · 2017Review
- Schizophrenia-associated methylomic variation: molecular signatures of disease and polygenic risk burden across multiple brain regions.Human molecular genetics · 2017Article
- Toward development of epigenetic drugs for central nervous system disorders: Modulating neuroplasticity via H3K4 methylation.Psychiatry and clinical neurosciences · 2016Review
- The Genetic Intersection of Neurodevelopmental Disorders and Shared Medical Comorbidities - Relations that Translate from Bench to Bedside.Frontiers in psychiatry · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The Psychiatric Genomics Consortium-Schizophrenia Workgroup (PGC-SCZ) recently identified 108 loci associated with increased risk for schizophrenia (SCZ). The vast majority of these variants reside within non-coding sequences of the genome and are predicted to exert their effects by affecting the mechanism of action of cis regulatory elements (CREs), such as promoters and enhancers. Although a number of large-scale collaborative efforts (e.g. ENCODE) have achieved a comprehensive mapping of CREs in human cell lines or tissue homogenates, it is becoming increasingly evident that many risk-associated variants are enriched for expression Quantitative Trait Loci (eQTLs) and CREs in specific tissues or cells. As such, data derived from previous research endeavors may not capture fully cell-type and/or region specific changes associated with brain diseases. Coupling recent technological advances in genomics with cell-type specific methodologies, we are presented with an unprecedented opportunity to better understand the genetics of normal brain development and function and, in turn, the molecular basis of neuropsychiatric disorders. In this review, we will outline ongoing efforts towards this goal and will discuss approaches with the potential to shed light on the mechanism(s) of action of cell-type specific cis regulatory elements and their putative roles in disease, with particular emphasis on understanding the manner in which the epigenome and CREs influence the etiology of SCZ.
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.