| http://purl.uniprot.org/citations/35544990 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/35544990 | http://www.w3.org/2000/01/rdf-schema#comment | "Abnormalities in Ca2+ homeostasis in Bipolar Disorders (BD) have been associated with impairments in glutamatergic receptors and voltage-gated calcium channels. Increased anterior cingulate cortex (ACC) glutamatergic neurometabolites have been consistently disclosed in BD by proton magnetic resonance spectroscopy (1H-MRS). A single nucleotide polymorphism (SNP) in the CACNA1C gene (rs1006737), which encodes the alpha 1-C subunit of the L-type calcium channel, has been associated with BD and is reported to modulate intra-cellular Ca2+. Thus, this study aimed to explore the association of the CACNA1C genotype with ACC glutamatergic metabolites measured by 1H-MRS in both BD and HC subjects. A total of 194 subjects (121 euthymic BD type I patients and 73 healthy controls (HC) were genotyped for CACNA1C rs1006737, underwent a 3-Tesla 1H-MRS imaging examination and ACC glutamatergic metabolite were assessed. We found overall increased glutamatergic metabolites in AA carriers in BD. Specifically, higher Glx/Cr was observed in subjects with the AA genotype compared to both AG and GG in the overall sample (BD + HC). Also, female individuals in the BD group with AA genotype were found to have higher Glx/Cr compared to those with other genotypes. CACNA1C AA carriers in use of anticonvulsant medication had higher estimated Glutamine (Glx-Glu) than the other genotypes. Thus, this study suggest an association between calcium channel genetics and increased glutamatergic metabolites in BD, possibly playing a synergic role in intracellular Ca2+ overload and excitotoxicity."xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.euroneuro.2022.04.001"xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/author | "Vallada H."xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/author | "Chile T."xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/author | "Soeiro-de-Souza M.G."xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/author | "Otaduy M.C.G."xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/author | "Scotti-Muzzi E."xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/name | "Eur Neuropsychopharmacol"xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/pages | "26-35"xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/title | "Association between CACNA1C gene rs100737 polymorphism and glutamatergic neurometabolites in bipolar disorder."xsd:string |
| http://purl.uniprot.org/citations/35544990 | http://purl.uniprot.org/core/volume | "59"xsd:string |
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