ReviewInternational journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience2011
The 22q11.2 microdeletion: fifteen years of insights into the genetic and neural complexity of psychiatric disorders.
Review in International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mental health dished up-the use of iPSC models in neuropsychiatric research.Journal of neural transmission (Vienna, Austria : 1996) · 2020Pooled it
- Developmentally dynamic, non-convergent transcriptomic profiles in CNV models for schizophrenia risk.Molecular psychiatry · 2026Article
- Hippocampal transcriptome profiling in a 22q11.2 deletion syndrome mouse model: comparison with human schizophrenia.Molecular brain · 2026Article
- Endothelial defects unveil cardiovascular phenotype in iPSC-based disease modelling across three generations of a DiGeorge syndrome family.Research square · 2025Article
- Synaptic-dependent developmental dysconnectivity in 22q11.2 deletion syndrome.Science advances · 2025Article
- Review of the Pathophysiology and Clinical Manifestations of 22q11.2 Deletion and Duplication Syndromes.Clinical reviews in allergy & immunology · 2025Review
- The relationship between COMT, proline, and negative symptoms in clinical high risk and recent psychosis onset.Translational psychiatry · 2024Article
- Synaptic-dependent developmental dysconnectivity in 22q11.2 deletion syndrome.bioRxiv : the preprint server for biology · 2024Article
- Toxoplasma gondii infection regulates apoptosis of host cells via miR-185/ARAF axis.Parasites & vectors · 2023Article
- Article
- Mitochondrial proteins encoded by the 22q11.2 neurodevelopmental locus regulate neural stem and progenitor cell proliferation.Molecular psychiatry · 2023Article
- Increased Central Auditory Gain and Decreased Parvalbumin-Positive Cortical Interneuron Density in theBiological psychiatry global open science · 2023Article
- A CRISPR-engineered isogenic model of the 22q11.2 A-B syndromic deletion.Scientific reports · 2023Article
- Mitochondrial genes in the 22q11.2 deleted region regulate neural stem and progenitor cell proliferation.bioRxiv : the preprint server for biology · 2023Article
- Hippocampal area CA2: interneuron disfunction during pathological states.Frontiers in neural circuits · 2023Review
- Review
- Enkephalin release from VIP interneurons in the hippocampal CA2/3a region mediates heterosynaptic plasticity and social memory.Molecular psychiatry · 2022Article
- Synaptic Plasticity Dysfunctions in the Pathophysiology of 22q11 Deletion Syndrome: Is There a Role for Astrocytes?International journal of molecular sciences · 2022Review
- Disparate insults relevant to schizophrenia converge on impaired spike synchrony and weaker synaptic interactions in prefrontal local circuits.Current biology : CB · 2022Article
- Social Cognition Impairments in 22q11.2DS Individuals With and Without Psychosis: A Comparison Study With a Large Population of Patients With Schizophrenia.Schizophrenia bulletin open · 2022Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Over the last fifteen years it has become established that 22q11.2 deletion syndrome (22q11DS) is a true genetic risk factor for schizophrenia. Carriers of deletions in chromosome 22q11.2 develop schizophrenia at rate of 25-30% and such deletions account for as many as 1-2% of cases of sporadic schizophrenia in the general population. Access to a relatively homogeneous population of individuals that suffer from schizophrenia as the result of a shared etiological factor and the potential to generate etiologically valid mouse models provides an immense opportunity to better understand the pathobiology of this disease. In this review we survey the clinical literature associated with the 22q11.2 microdeletions with a focus on neuroanatomical changes. Then, we highlight results from work modeling this structural mutation in animals. The key biological pathways disrupted by the mutation are discussed and how these changes impact the structure and function of neural circuits is described.
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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.