ReviewCNS neuroscience & therapeutics2011
Dysfunctional brain networks and genetic risk for schizophrenia: specific neurotransmitter systems.
Review in CNS neuroscience & therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 34 citations in OpenAlex.
- The utility of (11)C-arachidonate PET to study in vivo dopaminergic neurotransmission in humans.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Trial
- Shared Genetic Determinants of Schizophrenia and Autism Spectrum Disorder Implicate Opposite Risk Patterns: A Genome-Wide Analysis of Common Variants.Schizophrenia bulletin · 2024Article
- Male-biased vulnerability of mouse brain tryptophan/kynurenine and glutamate systems to adolescent exposures to concentrated ambient ultrafine particle air pollution.Neurotoxicology · 2024Article
- Short-chain fatty acids ameliorate imiquimod-induced skin thickening and IL-17 levels and alter gut microbiota in mice: a metagenomic association analysis.Scientific reports · 2024Article
- Are Essential Trace Elements Effective in Modulation of Mental Disorders? Update and Perspectives.Biological trace element research · 2022Review
- MicroRNAs in neuronal communication.Molecular neurobiology · 2014Review
- Mapping neurotransmitter networks with PET: an example on serotonin and opioid systems.Human brain mapping · 2014Article
- Epigenetics, stress, and their potential impact on brain network function: a focus on the schizophrenia diatheses.Frontiers in psychiatry · 2014Review
- Reduced expression of STOP/MAP6 in mice leads to cognitive deficits.Schizophrenia bulletin · 2013Article
- Agonist high- and low-affinity states of dopamine D₂ receptors: methods of detection and clinical implications.Naunyn-Schmiedeberg's archives of pharmacology · 2013Review
- The DTNBP1 (dysbindin-1) gene variant rs2619522 is associated with variation of hippocampal and prefrontal grey matter volumes in humans.European archives of psychiatry and clinical neuroscience · 2013Article
- Article
- Allosteric modulators for the treatment of schizophrenia: targeting glutamatergic networks.Current topics in medicinal chemistry · 2013Review
- Beyond dopamine: glutamate as a target for future antipsychotics.ISRN pharmacology · 2012Article
- Schizophrenia diagnosis and treatment.CNS neuroscience & therapeutics · 2011Article
- Mass spectrometry imaging of amino neurotransmitters: a comparison of derivatization methods and application in mouse brain tissue.Metabolomics : Official journal of the Metabolomic SocietyArticle
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple neurotransmitter circuits are disturbed in schizophrenia, and the dopamine hypothesis of schizophrenia prevails as the hypothesis with most empirical support. On the other hand, schizophrenia is highly heritable with a pattern consistent with both common and rare allelic variants and gene × environment interaction. Advances in the field of neuroimaging have expanded our knowledge of intermediate phenotypes, the neurobiological processes that convey the risk from the genes to the complex phenotype. In this article, we review the recent and continuously accumulating evidence from in vivo imaging studies aiming at characterizing neurochemical intermediate phenotypes of schizophrenia. Dopaminergic alterations in schizophrenia are shared by individuals at genetic risk who do not express the illness, suggesting a "dopamine hypothesis of schizophrenia vulnerability." This hypothesis has the potential to help us better understand the dopaminergic dysfunction in the context of the complex pathophysiological process leading to schizophrenia. In the future, neurotransmitter imaging studies should investigate the gene × environment interaction in schizophrenia, and try to identify neurobiological correlates of heightened sensitivity to environmental stressors (e.g., cannabis, childhood trauma, and other psychosocial stress) in genetically vulnerable individuals.
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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.