ReviewNeural plasticity2012
Animal models of psychiatric disorders that reflect human copy number variation.
Review in Neural plasticity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed.
- Eating behaviour and eating disorders in individuals with rare neurodevelopmental variants: current knowledge and future research directions.Frontiers in psychiatry · 2025Article
- Genetically modified mice as a tool for the study of human diseases.Molecular biology reports · 2024Review
- Chromosomal Microarray Analysis as First-Tier Genetic Test for Schizophrenia.Frontiers in genetics · 2021Article
- From Multisensory Assessment to Functional Interpretation of Social Behavioral Phenotype in Transgenic Mouse Models for Autism Spectrum Disorders.Frontiers in psychiatry · 2020Review
- Endogenous Retroviruses Activity as a Molecular Signature of Neurodevelopmental Disorders.International journal of molecular sciences · 2019Review
- High resolution analysis of rare copy number variants in patients with autism spectrum disorder from Taiwan.Scientific reports · 2017Article
- Transcriptome profiling of white adipose tissue in a mouse model for 15q duplication syndrome.Genomics data · 2015Article
- Genomic structural variation in affective, anxiety, and stress-related disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2015Review
- Advancing the discovery of medications for autism spectrum disorder using new technologies to reveal social brain circuitry in rodents.Psychopharmacology · 2014Review
- Altered social behaviours in neurexin 1α knockout mice resemble core symptoms in neurodevelopmental disorders.PloS one · 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of genetic technologies has led to the identification of several copy number variations (CNVs) in the human genome. Genome rearrangements affect dosage-sensitive gene expression in normal brain development. There is strong evidence associating human psychiatric disorders, especially autism spectrum disorders (ASDs) and schizophrenia to genetic risk factors and accumulated CNV risk loci. Deletions in 1q21, 3q29, 15q13, 17p12, and 22q11, as well as duplications in 16p11, 16p13, and 15q11-13 have been reported as recurrent CNVs in ASD and/or schizophrenia. Chromosome engineering can be a useful technology to reflect human diseases in animal models, especially CNV-based psychiatric disorders. This system, based on the Cre/loxP strategy, uses large chromosome rearrangement such as deletion, duplication, inversion, and translocation. Although it is hard to reflect human pathophysiology in animal models, some aspects of molecular pathways, brain anatomy, cognitive, and behavioral phenotypes can be addressed. Some groups have created animal models of psychiatric disorders, ASD, and schizophrenia, which are based on human CNV. These mouse models display some brain anatomical and behavioral abnormalities, providing insight into human neuropsychiatric disorders that will contribute to novel drug screening for these devastating disorders.
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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.