The aim of the study is to investigate the effect of a glutamate transporter polymorphism EAAT2-181A > C (rs4354668) and exposure to ACE on white matter microstructure in patients with BD.
This study thus focused on epigenetic DNA methylation regulation of <i>SLC1A2</i>, encoding for EAAT2, in BD with variable environmental influences of addiction.
The coding and putative regulatory regions of SLC1A2 gene were screened for variants using high resolution melting or sequenced in 1099 or in 32 BD subjects.
The aim of the study is to investigate the effect of glutamate transporter polymorphism SLC1A2-181A>C and exposure to Adverse Childhood Experiences (ACE) on hippocampal gray matter volume of patients with bipolar disorder (BD).
The aim of the study is to investigate the effect of glutamate transporter polymorphism SLC1A2-181A>C and exposure to Adverse Childhood Experiences (ACE) on hippocampal gray matter volume of patients with bipolar disorder (BD).
In this postmortem study we used in situ hybridization and microarray analysis to evaluate the gene expression of the membrane transporters SLC1A2 and SLCA3 and the vesicular transporter SLCA17A7 in the hippocampus of Major Depressive Disorder (MDD) and Bipolar Disorder (BPD) subjects.
In this postmortem study we used in situ hybridization and microarray analysis to evaluate the gene expression of the membrane transporters SLC1A2 and SLCA3 and the vesicular transporter SLCA17A7 in the hippocampus of Major Depressive Disorder (MDD) and Bipolar Disorder (BPD) subjects.
Patients were genotyped for SLC1A2 -181A>C by polymerase chain reaction-restriction fragment length polymorphism, and the influence of genotype on BD episode recurrence rates, and the interaction between the single nucleotide polymorphism and lithium treatment, were analyzed.
The aims of the study were to investigate if factors affecting glutamate function, such as SLC1A2 -181A>C (rs4354668), could affect recurrence of illness in BD, and if they interact with lithium salt treatment.
With probes designed for the human EAAT1, EAAT2, EAAT3, and EAAT4 transcripts, we performed in situ hybridization and detected decreased expression of EAAT3 and EAAT4 transcripts in the striatum in bipolar disorder.