Publications by authors named "Gulja Babadjanova"

Article Synopsis
  • Bipolar disorder has a genetic basis and complex causes; a large study compared nearly 42,000 bipolar patients with over 371,000 healthy controls, revealing 64 genomic regions linked to the disorder.
  • The findings showed that risk-related genes are heavily associated with brain functions, particularly in areas like the prefrontal cortex and hippocampus, and they include targets for various medications.
  • The research also distinguished between bipolar disorder types I and II, revealing a close genetic relationship and highlighting 15 specific genes that could lead to new treatment options and further investigations.
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Background: Bipolar disorder (BD) is a common and highly heritable disorder of mood. Genome-wide association studies (GWAS) have identified several independent susceptibility loci. In order to extract more biological information from GWAS data, multi-locus approaches represent powerful tools since they utilize knowledge about biological processes to integrate functional sets of genes at strongly to moderately associated loci.

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Article Synopsis
  • Bipolar disorder (BD) is a highly hereditary mental illness marked by alternating episodes of mania and depression, sharing significant genetic and clinical traits with schizophrenia (SCZ).
  • A study involving a large dataset of BD patients and controls found that 22 out of 107 genetic variants (SNPs) identified in SCZ research showed a link to BD, indicating shared genetic risk factors.
  • Notably, one significant SNP was near the TRANK1 gene, known to be associated with BD; this study also highlighted potential disease pathways involving calcium and glutamate signaling, which could lead to new treatment strategies for both disorders.
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Bipolar disorder (BD) is a common and highly heritable mental illness and genome-wide association studies (GWAS) have robustly identified the first common genetic variants involved in disease aetiology. The data also provide strong evidence for the presence of multiple additional risk loci, each contributing a relatively small effect to BD susceptibility. Large samples are necessary to detect these risk loci.

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Background: Common genetic polymorphisms at chromosome 3p21.1, including rs2251219 in polybromo 1 (PBRM1), have been implicated in susceptibility to bipolar affective disorder (BP) through genome-wide association studies. Subsequent studies have suggested that this is also a risk locus for other psychiatric phenotypes, including major depression and schizophrenia.

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We conducted a genome-wide association study (GWAS) and a follow-up study of bipolar disorder (BD), a common neuropsychiatric disorder. In the GWAS, we investigated 499,494 autosomal and 12,484 X-chromosomal SNPs in 682 patients with BD and in 1300 controls. In the first follow-up step, we tested the most significant 48 SNPs in 1729 patients with BD and in 2313 controls.

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Background/aims: A strong association has been confirmed between age-related macular degeneration (AMD) and variants at two independent loci including Tyr402His in the complement factor H (CFH) on 1q32 and Ser69Ala at LOC387715, a hypothetical gene on chromosome 10q26. The contribution of both loci to AMD was investigated in an isolated north-west Russian population.

Methods: Together with a PLEKHA1 variant at 10q26, the CFH Tyr402His and LOC387715 Ser69Ala polymorphisms were genotyped in 155 patients with AMD and 151 age-matched controls.

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