ReviewBrain research2017
Using hiPSCs to model neuropsychiatric copy number variations (CNVs) has potential to reveal underlying disease mechanisms.
Review in Brain research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Chromosomal Microarray Analysis as First-Tier Genetic Test for Schizophrenia.Frontiers in genetics · 2021Article
- METTL1-mediated mStem cell research & therapy · 2020Article
- Investigation of Schizophrenia with Human Induced Pluripotent Stem Cells.Advances in neurobiology · 2020Review
- From enhanceropathies to the epigenetic manifold underlying human cognition.Human molecular genetics · 2019Review
- The use of brain organoids to investigate neural development and disease.Nature reviews. Neuroscience · 2017Review
- Application of CRISPR/Cas9 to the study of brain development and neuropsychiatric disease.Molecular and cellular neurosciences · 2017Review
- The promises and challenges of human brain organoids as models of neuropsychiatric disease.Nature medicine · 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
2 authors.
Funding
Abstract
Schizophrenia is a neuropsychological disorder with a strong heritable component; genetic risk for schizophrenia is conferred by both common variants of relatively small effect and rare variants with high penetrance. Genetically engineered mouse models can recapitulate rare variants, displaying some behavioral defects associated with schizophrenia; however, these mouse models cannot recapitulate the full genetic architecture underlying the disorder. Patient-derived human induced pluripotent stem cells (hiPSCs) present an alternative approach for studying rare variants, in the context of all other risk alleles. Genome editing technologies, such as CRISPR-Cas9, enable the generation of isogenic hiPSC lines with which to examine the functional contribution of single variants within any genetic background. Studies of these rare variants using hiPSCs have the potential to identify commonly disrupted pathways in schizophrenia and allow for the identification of new therapeutic targets. This article is part of a Special Issue entitled SI:StemsCellsinPsychiatry.
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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.