ArticleNeuropsychiatric disease and treatment2015
Increased expression of retinoic acid-induced gene 1 in the dorsolateral prefrontal cortex in schizophrenia, bipolar disorder, and major depression.
Article in Neuropsychiatric disease and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
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Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.
- Retinoic Acid-Induced 1 Gene and Neuropsychiatric Diseases: A Systematic Review.Expert reviews in molecular medicine · 2025Pooled it
- Meta-analysis of genomic variants and gene expression data in schizophrenia suggests the potential need for adjunctive therapeutic interventions for neuropsychiatric disorders.Journal of genetics · 2019Pooled it
- Neurocognitive Graphs of First-Episode Schizophrenia and Major Depression Based on Cognitive Features.Neuroscience bulletin · 2018Trial
- Retinoic Acid Induced 1 and Smith-Magenis Syndrome: From Genetics to Biology and Possible Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Brain Specific RagA Overexpression Triggers Depressive-Like Behaviors in Mice via Activating ADORA2A Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- Retinoid homeostasis in major depressive disorder.Translational psychiatry · 2023Article
- Neuron-Microglia Crosstalk in Neuropsychiatric Disorders.Advances in experimental medicine and biology · 2023Review
- Article
- Targeting Mitochondrial Dysfunction for Bipolar Disorder.Current topics in behavioral neurosciences · 2021Review
- Manipulation of retinoic acid signaling in the nucleus accumbens shell alters rat emotional behavior.Behavioural brain research · 2019Article
- Mitochondrial Agents for Bipolar Disorder.The international journal of neuropsychopharmacology · 2018Review
- Review
- Targeting Retinoid Receptors to Treat Schizophrenia: Rationale and Progress to Date.CNS drugs · 2016Review
- Evidence for genetic regulation of mRNA expression of the dosage-sensitive gene retinoic acid induced-1 (RAI1) in human brain.Scientific reports · 2016Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRetinoids regulate gene expression in different cells and tissues at the transcriptional level. Retinoic acid transcriptionally regulates downstream regulatory molecules, including enzymes, transcription factors, cytokines, and cytokine receptors. Animal models indicate an involvement of retinoid signaling pathways in the regulation of synaptic plasticity and learning, especially in the hippocampus. Retinoic acid-inducible or induced gene 1 (RAI-1) is induced during neuronal differentiation, and was associated with the severity of the phenotype and response to medication in schizophrenic patients.
methodsIn the present study, we used immunohistochemistry to investigate the expression of RAI-1 in 60 brains from the Stanley Neuropathology Consortium (15 cases each from controls and from patients with schizophrenia, bipolar disorder, and major depression). Rating scores for density and intensity were determined in the dorsolateral prefrontal cortex.
resultsAll four groups showed high interindividual variation. RAI-1-positive cells were identified as neurons and astrocytes. Significantly increased intensities in cortical neurons were noted in all three major psychiatric groups compared with controls. The density of RAI-1-positive neurons was increased (P=0.06) in schizophrenia and bipolar disorder. In bipolar disorder, RAI-1-positive astrocytes in gray matter showed a significantly increased intensity and compound value. Thus, a significant increase in the parameters measured was found in schizophrenia, bipolar disorder, and major depression.
conclusionOur study shows a significant increase in expression of RAI-1 in the brains from patients with schizophrenia, bipolar disorder, or major depression. The increased expression might reflect altered signaling pathways, like that for retinoic acid. The underlying mechanisms leading to the increased expression and its functional consequences are so far unknown, and remain to be investigated in future studies.
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