ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry2014
A Synaptic Function Approach to Investigating Complex Psychiatric Diseases.
Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Tbx1 haploinsufficiency leads to local skull deformity, paraflocculus and flocculus dysplasia, and motor-learning deficit in 22q11.2 deletion syndrome.Nature communications · 2024Article
- A novel role for phospholamban in the thalamic reticular nucleus.Scientific reports · 2024Article
- Neuroinflammation and Oxidative Stress in Individuals Affected by DiGeorge Syndrome.International journal of molecular sciences · 2023Review
- Therapeutic Implications of microRNAs in Depressive Disorders: A Review.International journal of molecular sciences · 2022Review
- Chronic but not acute pharmacological activation of SERCA induces behavioral and neurochemical effects in male and female mice.Behavioural brain research · 2021Article
- A Case for Thalamic Mechanisms of Schizophrenia: Perspective From Modeling 22q11.2 Deletion Syndrome.Frontiers in neural circuits · 2021Review
- Dendritic Spine Plasticity: Function and Mechanisms.Frontiers in synaptic neuroscience · 2020Article
- Dissociable Disruptions in Thalamic and Hippocampal Resting-State Functional Connectivity in Youth with 22q11.2 Deletions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Long-Term Plasticity of Neurotransmitter Release: Emerging Mechanisms and Contributions to Brain Function and Disease.Annual review of neuroscience · 2018Review
- The SERCA2: A Gatekeeper of Neuronal Calcium Homeostasis in the Brain.Cellular and molecular neurobiology · 2018Review
- Mitochondria in complex psychiatric disorders: Lessons from mouse models of 22q11.2 deletion syndrome: Hemizygous deletion of several mitochondrial genes in the 22q11.2 genomic region can lead to symptoms associated with neuropsychiatric disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017Review
- Thalamic miR-338-3p mediates auditory thalamocortical disruption and its late onset in models of 22q11.2 microdeletion.Nature medicine · 2017Article
- Weaving a Net of Neurobiological Mechanisms in Schizophrenia and Unraveling the Underlying Pathophysiology.Biological psychiatry · 2016Review
- 22q11.2 deletion syndrome.Nature reviews. Disease primers · 2015Review
- Dysplasticity, metaplasticity, and schizophrenia: Implications for risk, illness, and novel interventions.Development and psychopathology · 2015Review
- Perineuronal nets and schizophrenia: the importance of neuronal coatings.Neuroscience and biobehavioral reviews · 2014Review
- Non-coding RNA regulation of synaptic plasticity and memory: implications for aging.Ageing research reviews · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The 22q11 deletion syndrome (22q11DS) is the most common microdeletion syndrome in humans and presents with a complex and variable psychiatric phenotype. Patients show cognitive impairment and have a higher probability of psychiatric disorders. As much as 30% of patients with 22q11DS suffer from schizophrenia, the strongest association between any mutation and the disease. Schizophrenia is a complex psychiatric disease that affects multiple brain regions, giving rise to a constellation of seemingly unrelated symptoms including hallucinations, social withdrawal, and memory deficits. Synaptic or neuronal malfunctions within certain physiological circuits appear to be at the core of these symptoms. Understanding disease at the synaptic level requires genetic model systems where intact neural circuits can be interrogated for functional deficits. Because of the overlap between 22q11DS and schizophrenia, models of 22q11DS may be key genetic tools for investigating both diseases. Here we discuss the advantages of using a synaptic function approach to studying mouse models of 22q11DS, review recent findings, and discuss them in the broader context of 22q11DS and schizophrenia.
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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.