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SLC6A4 variation and citalopram response.

Publication ,  Journal Article
Mrazek, DA; Rush, AJ; Biernacka, JM; O'Kane, DJ; Cunningham, JM; Wieben, ED; Schaid, DJ; Drews, MS; Courson, VL; Snyder, KA; Black, JL ...
Published in: Am J Med Genet B Neuropsychiatr Genet
April 5, 2009

The influence of genetic variations in SLC6A4 (serotonin transporter gene) on citalopram treatment of depression using the Sequenced Treatment to Relieve Depression (STAR*D) sample was assessed. Of primary interest were three previously studied polymorphisms: 1) the VNTR variation of the second intron, 2) the indel promoter polymorphism (5HTTLPR or SERT), and 3) a single nucleotide polymorphism (SNP) rs25531. Additionally, SLC6A4 was resequenced to identify new SNPs for exploratory analyses. DNA from 1914 subjects in the STAR*D study were genotyped for the intron 2 VNTR region, the indel promoter polymorphism, and rs25531. Associations of these variants with remission of depressive symptoms were evaluated following citalopram treatment. In white non-Hispanic subjects, variations in the intron 2 VNTR (point-wise P = 0.041) and the indel promoter polymorphism (point-wise P = 0.039) were associated with remission following treatment with citalopram. The haplotype composed of the three candidate loci was also associated with remission, with a global p-value of 0.040 and a maximum statistic simulation p-value of 0.0031 for the S-a-12 haplotype, under a dominant model. One SNP identified through re-sequencing the SLC6A4 gene, Intron7-83-TC, showed point-wise evidence of association, which did not remain significant after correction for the number of SNPs evaluated in this exploratory analysis. No associations between these SLC6A4 variations and remission were found in the white Hispanic or black subjects. These findings suggest that multiple variations in the SLC6A4 gene are associated with remission in white non-Hispanic depressed adults treated with citalopram. The mechanism of action of these variants remains to be determined.

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Published In

Am J Med Genet B Neuropsychiatr Genet

DOI

EISSN

1552-485X

Publication Date

April 5, 2009

Volume

150B

Issue

3

Start / End Page

341 / 351

Location

United States

Related Subject Headings

  • White People
  • Treatment Outcome
  • Serotonin Plasma Membrane Transport Proteins
  • Sequence Analysis, DNA
  • Selective Serotonin Reuptake Inhibitors
  • Remission Induction
  • Promoter Regions, Genetic
  • Polymorphism, Single Nucleotide
  • Minisatellite Repeats
  • Middle Aged
 

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Mrazek, D. A., Rush, A. J., Biernacka, J. M., O’Kane, D. J., Cunningham, J. M., Wieben, E. D., … Weinshilboum, R. M. (2009). SLC6A4 variation and citalopram response. Am J Med Genet B Neuropsychiatr Genet, 150B(3), 341–351. https://doi.org/10.1002/ajmg.b.30816
Mrazek, D. A., A. J. Rush, J. M. Biernacka, D. J. O’Kane, J. M. Cunningham, E. D. Wieben, D. J. Schaid, et al. “SLC6A4 variation and citalopram response.Am J Med Genet B Neuropsychiatr Genet 150B, no. 3 (April 5, 2009): 341–51. https://doi.org/10.1002/ajmg.b.30816.
Mrazek DA, Rush AJ, Biernacka JM, O’Kane DJ, Cunningham JM, Wieben ED, et al. SLC6A4 variation and citalopram response. Am J Med Genet B Neuropsychiatr Genet. 2009 Apr 5;150B(3):341–51.
Mrazek, D. A., et al. “SLC6A4 variation and citalopram response.Am J Med Genet B Neuropsychiatr Genet, vol. 150B, no. 3, Apr. 2009, pp. 341–51. Pubmed, doi:10.1002/ajmg.b.30816.
Mrazek DA, Rush AJ, Biernacka JM, O’Kane DJ, Cunningham JM, Wieben ED, Schaid DJ, Drews MS, Courson VL, Snyder KA, Black JL, Weinshilboum RM. SLC6A4 variation and citalopram response. Am J Med Genet B Neuropsychiatr Genet. 2009 Apr 5;150B(3):341–351.
Journal cover image

Published In

Am J Med Genet B Neuropsychiatr Genet

DOI

EISSN

1552-485X

Publication Date

April 5, 2009

Volume

150B

Issue

3

Start / End Page

341 / 351

Location

United States

Related Subject Headings

  • White People
  • Treatment Outcome
  • Serotonin Plasma Membrane Transport Proteins
  • Sequence Analysis, DNA
  • Selective Serotonin Reuptake Inhibitors
  • Remission Induction
  • Promoter Regions, Genetic
  • Polymorphism, Single Nucleotide
  • Minisatellite Repeats
  • Middle Aged