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AB0015 Association between bdnf, ntrk2 and creb1 gene polymorphisms and fibromyalgia
  1. S.-S. Nah1,
  2. S. S. Jeong2,
  3. S.-K. Kim3,
  4. S.-H. Kim4,
  5. Y.-A. Lee5,
  6. J. H. Lee6,
  7. S.-J. Hong5,
  8. H.-S. Kim7,
  9. H.-S. Lee8,
  10. H. A. Kim9,
  11. C.-I. Joung10,
  12. H.-I. Yang5,
  13. J.-W. Hur11,
  14. S. H. Kim12,
  15. S.-S. Lee13
  1. 1Division Of Rheumatology, Department Of Internal Medicine, Soonchunhyang University, College Of Medicine, Choenan
  2. 2Department psychiatry, Bright future clinic, Seoul
  3. 3Division Of Rheumatology, Department Of Internal Medicine, Catholic University of Daegu School of Medicine, Daegu
  4. 4Division Of Rheumatology, Department Of Internal Medicine, Inje University Haeundae Paik Hospital, Busan
  5. 5Division Of Rheumatology, Department Of Internal Medicine, Kyung Hee University, Seoul
  6. 6Division Of Rheumatology, Department Of Internal Medicine, Maryknoll Medical Center, Busan
  7. 7Division Of Rheumatology, Department Of Internal Medicine, Chosun University, Gwangju
  8. 8Division Of Rheumatology, Department Of Internal Medicine, Hanyang University College of Medicine, Seoul
  9. 9Division Of Rheumatology, Department Of Internal Medicine, Ajou University Hospital, Suwon
  10. 10Division Of Rheumatology, Department Of Internal Medicine, Konyang University Medical School, Daejeon
  11. 11Division Of Rheumatology, Department Of Internal Medicine, Eulji university hospital, Seoul
  12. 12Division Of Rheumatology, Department Of Internal Medicine, Gyemung university hospital, Daegu
  13. 13Division Of Rheumatology, Department Of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea, Republic Of

Abstract

Background Studies over the past 20 years have shown that fibromyalgia (FM) is a pain amplification disorder with clear evidence for a pathogenesis within the central nervous system. Brain-derived neurotrophic factor (BDNF) signaling pathway participates in plasticity mechanisms and serves as a neurotransmitter modulator. The pathway includes cyclic adenosine monophosphate response element-binding protein 1 (CREB1), BDNF, and its receptor (neurotrophic tyrosine kinase receptor, type 2 [NTRK2]). The variations of the genes were known to be associated with human neuropsychiatric disorders.

Objectives We proposed to determine whether these BDNF-NTRK2-CREB1 pathway gene single nucleotide polymorphisms (SNPs) were associated with FM and/or any of its clinical variables.

Methods Patients with FM (N = 422) and age-sex matched healthy normal controls (HNC, N = 410) were studied. Patients were carefully diagnosed by well trained rheumatologists at 13 tertiary hospitals. The SNPs were determined using Taq-Man analysis. In this study, three SNPs of BDNF (rs6265), NTRK2 (rs1187323), and CREB1 (rs2253206) genes were selected for the analysis. The patients and control groups were compared using case-control association analysis. The χ2 test was used to estimate the Hardy-Weinberg equilibrium (HWE). Allele frequency was defined as the percentage of the individuals carrying the allele among the total number of the individuals. Logistic regression analyses were used to calculate odds ratios (95% confidence interval). A P-value of less than 0.05 was considered to indicate statistical significance.

Results Of the SNPs, CREB1 gene SNP (rs2253206) is statistically associated with the susceptibility of FM. The CREB1 SNP distribution was 150 (36%) GG, 204 (48%) GA, and 68 (16%) AA for HNC and 173 (42%) GG, 187(46%) GA, and 50 (12%) AA for HNC, respectively (Table 1).

Conclusions This is the first study to associate the BDNF-NTRK2-CREB1 pathway gene polymorphisms with FM and its subgroup phenotype.

  1. Castren E, Voikar V, Rantamaki T (2006): Role of neurotrophic factors in depression. Curr Opin Pharmacol 7:18 –21.

  2. Duman RS, Monteggia LM (2006): A neurotrophic model for stressrelated mood disorders. Biol Psychiatry 59:1116 –1127.

  3. Carlson PJ, Singh JB, Zarate CA Jr, Drevets WC, Manji HK (2006): Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets. NeuroRx 3:22– 41.

Disclosure of Interest None Declared

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