ReviewFrontiers in cellular neuroscience2016
Epigenetic RELN Dysfunction in Schizophrenia and Related Neuropsychiatric Disorders.
Review in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.
- Association Between REELIN Gene Polymorphisms (rs7341475 and rs262355) and Risk of Schizophrenia: an Updated Meta-analysis.Journal of molecular neuroscience : MN · 2021Pooled it
- Dissecting the Epigenetic Changes Induced by Non-Antipsychotic Mood Stabilizers on Schizophrenia and Affective Disorders: A Systematic Review.Frontiers in pharmacology · 2020Pooled it
- Trial
- Alterations in GABAergic Interneurons, Neuroinflammation, and Epigenetics: Potential Targets for Therapeutic Strategies in Schizophrenia.Current neuropharmacology · 2026Article
- Exploring the roots of schizophrenia: Current research and future directions (Review).Experimental and therapeutic medicine · 2026Review
- Polydopamine-Based Antioxidant Countermeasures Against Spaceflight-Induced Neurodegeneration.Small science · 2026Article
- ADAMTS2: More than a procollagen N-proteinase.Genes & diseases · 2025Review
- G9a an Epigenetic Therapeutic Strategy for Neurodegenerative Conditions: From Target Discovery to Clinical Trials.Medicinal research reviews · 2025Review
- miRNA-Based Diagnosis of Schizophrenia Using Machine Learning.International journal of molecular sciences · 2025Article
- Dysregulation of Serum Exosomal Lipid Metabolism in Schizophrenia: A Biomarker Perspective.Molecular neurobiology · 2025Article
- Epigenetics Modulators as Therapeutics for Neurological Disorders.Current pharmaceutical design · 2025Review
- Epigenetic Control in Schizophrenia.Sub-cellular biochemistry · 2025Review
- Regulatory mechanism of Reelin activity: a platform for exploiting Reelin as a therapeutic agent.Frontiers in molecular neuroscience · 2025Review
- Article
- Molecular Mechanisms of Reelin in the Enteric Nervous System and the Microbiota-Gut-Brain Axis: Implications for Depression and Antidepressant Therapy.International journal of molecular sciences · 2024Review
- HeterozygouseNeuro · 2023Article
- Maternal Immune Activation Induces Adolescent Cognitive Deficits Preceded by Developmental Perturbations in Cortical Reelin Signalling.Biomolecules · 2023Article
- Neurobiological Highlights of Cognitive Impairment in Psychiatric Disorders.International journal of molecular sciences · 2022Review
- Working memory deficits in children with schizophrenia and its mechanism, susceptibility genes, and improvement: A literature review.Frontiers in psychiatry · 2022Review
- Identification of Novel Genetic Variants Associated with Insomnia and Migraine Comorbidity.Nature and science of sleep · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
REELIN (RELN) is a large (420 kDa) glycoprotein that in adulthood is mostly synthesized in GABAergic neurons of corticolimbic structures. Upon secretion in the extracellular matrix (ECM), RELN binds to VLDL, APOE2, and α3β2 Integrin receptors located on dendritic shafts and spines of postsynaptic pyramidal neurons. Reduced levels of RELN expression in the adult brain induce cognitive impairment and dendritic spine density deficits. RELN supplementation recovers these deficits suggesting a trophic action for RELN in synaptic plasticity. We and others have shown that altered RELN expression in schizophrenia (SZ) and bipolar (BP) disorder patients is difficult to reconcile with classical Mendelian genetic disorders and it is instead plausible to associate these disorders with altered epigenetic homeostasis. Support for the contribution of altered epigenetic mechanisms in the down-regulation of RELN expression in corticolimbic structures of psychotic patients includes the concomitant increase of DNA-methyltransferases and the increased levels of the methyl donor S-adenosylmethionine (SAM). It is hypothesized that these conditions lead to RELN promoter hypermethylation and a reduction in RELN protein amounts in psychotic patients. The decreased synthesis and release of RELN from GABAergic corticolimbic neurons could serve as a model to elucidate the epigenetic pathophysiological mechanisms acting at pyramidal neuron dendrites that regulate synaptic plasticity and cognition in psychotic and non-psychotic subjects.
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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.