GABAergic promoter hypermethylation as a model to study the neurochemistry of schizophrenia vulnerability
Autor: | Ekrem Maloku, Dennis R. Grayson, W. B. Ruzicka, Ying Chen, Rosalba Satta, Alessandro Guidotti, Erbo Dong, Marin Veldic, Erminio Costa, Marija Kundakovic, Adrian Zhubi |
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Rok vydání: | 2009 |
Předmět: |
Psychosis
medicine.drug_class Cell Adhesion Molecules Neuronal medicine.medical_treatment Nerve Tissue Proteins Pharmacology Chromatin remodeling Epigenesis Genetic medicine Animals Humans Genetic Predisposition to Disease Pharmacology (medical) Epigenetics Promoter Regions Genetic Antipsychotic gamma-Aminobutyric Acid Clozapine Neurons Extracellular Matrix Proteins Glutamate Decarboxylase business.industry General Neuroscience Serine Endopeptidases Histone deacetylase inhibitor Brain DNA Methylation medicine.disease Reelin Protein Gene Expression Regulation Schizophrenia Neurology (clinical) business Sulpiride Antipsychotic Agents medicine.drug |
Zdroj: | Expert Review of Neurotherapeutics. 9:87-98 |
ISSN: | 1744-8360 1473-7175 |
Popis: | The neuronal GABAergic mechanisms that mediate the symptomatic beneficial effects elicited by a combination of antipsychotics with valproate (a histone deacetylase inhibitor) in the treatment of psychosis (expressed by schizophrenia or bipolar disorder patients) are unknown. This prompted us to investigate whether the beneficial action of this combination results from a modification of histone tail covalent esterification or is secondary to specific chromatin remodeling. The results suggest that clozapine, or sulpiride associated with valproate, by increasing DNA demethylation with an unknown mechanism, causes a chromatin remodeling that brings about a beneficial change in the epigenetic GABAergic dysfunction typical of schizophrenia and bipolar disorder patients. |
Databáze: | OpenAIRE |
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