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Association of the glutamate transporter gene SLC1A1 with atypical antipsychotics-induced obsessive-compulsive

Jun Soo Kwon1, Yeon Ho Joo, Hee Jung Nam

  • 1Department of Neuropsychiatry, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Korea.

Archives of General Psychiatry
|November 4, 2009
PubMed
Abstract

Insights

Genetic variations in the SLC1A1 gene are linked to atypical antipsychotic-induced obsessive-compulsive symptoms in schizophrenia patients. This study explores the genetic basis of these symptoms, offering insights into treatment mechanisms.

Area of Science:

  • Neuroscience
  • Pharmacogenetics
  • Psychiatry

Background:

  • Atypical antipsychotics (AAP) are known to induce obsessive-compulsive (OC) symptoms.
  • The underlying mechanisms remain largely unexplored.
  • Genetic association studies offer a viable approach to investigate the molecular basis of AAP-induced OC symptoms.

Purpose of the Study:

  • To investigate the association between polymorphisms in the glutamate transporter gene SLC1A1 and AAP-induced OC symptoms in schizophrenia patients.
  • To identify potential genetic markers for susceptibility to these adverse effects.

Main Methods:

  • A pharmacogenetic case-control association study was conducted.
  • Patients with schizophrenia receiving AAP treatment were analyzed (n=94).
  • Allele, genotype, and haplotype frequencies of SLC1A1 were assessed using logistic regression.

Main Results:

  • Trends of association were observed for specific SNPs (rs2228622, rs3780412) in the SLC1A1 gene.
  • A significant association was found for the A/C/G haplotype (rs2228622-rs3780413-rs3780412) with AAP-induced OC symptoms, which withstood multiple testing correction.
  • The odds ratio for the associated haplotype was 3.955.

Conclusions:

  • Sequence variations in SLC1A1 are associated with susceptibility to AAP-induced OC symptoms.
  • This is the first pharmacogenetic study to demonstrate this association.
  • Findings suggest the involvement of glutamatergic neurotransmission in the development of AAP-induced OC symptoms.

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