Association between genetic variants of GRM7 (rs1396409 and rs9883258) and treatment outcomes in Schizophrenic Egyptian patients

Abstract

Background and Aim

This study evaluated the association between rs1396409 and rs9883258 and the risk of schizophrenia (SCZ) and treatment outcomes in Egyptian patients.

Methods

This study included 88 patients with SCZ and 88 healthy controls. Lipid profile was assayed. Genotyping of rs1396409 and rs9883258 polymorphisms was analyzed using real-time PCR.

Results

The rs1396409 AG genotype frequency was significantly associated with SCZ risk (p = 0.002). Also, significant increased risk of SCZ was observed under allelic (p = 0.001), dominant (p = 0.001) and overdominant (p = 0.001) genetic model of rs1396409. However, rs9883258 AA genotype revealed nonsignificant association with SCZ. Cases with the rs1396409AG genotype exhibited hypertriglyceridemia (p < 0.001) and hypercholesterolemia (p = 0.001). In total, 72.3% and 74.5% of the cases presented with rs1396409 AG have negative symptoms (p = 0.022) and exhibited poor drug response (p = 0.023), respectively; all cases with rs1396409 GG genotype attempted suicide (p = 0.002) and are drug-free (p = 0.003). SCZ patients with negative symptoms had hypercholesterolemia (p = 0.008) mainly low-density lipoproteins (LDLc) (p = 0.016), and those with cognitive symptoms presented with low level of high-density lipoprotein (HDLc) (p = 0.023). Moreover, the multivariate regression analysis revealed that both rs1396409 G allele and HDLc were predictors of SCZ (p = 0.003 and 0.001, resp.).

Conclusion

The current study concluded that metabotropic glutamate receptor 7 (GRM7) rs1396409 AG could be a potential biomarker for SCZ diagnosis. It also revealed an independent association between the GRM7 rs1396409 G allele, HDLc and SCZ development.

Keywords:

• GRM7
• schizophrenia
• polymorphism
• real-time PCR
• dyslipidemia

Disclosure statement

The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

Authors’ contributions

Abeer A. Alrefai and Shimaa E. Soliman completed the genetic analysis. Ahmed N. Ramadan collected data. Yasser Abdelsattar and Marwa M. Omar analyzed and interpreted the results. All the authors reviewed and approved the final manuscript after contributing to its writing and editing. The authors state that no paper mill was utilized and that all data were generated internally.

Ethical approval and consent to participate

The procedures used in studies involving human subjects complied with the Declaration of Helsinki and were approved by the Menoufia University Faculty of Medicine’s ethical committee. All individuals taking part in the study gave their informed consent.

Competing interests

None of the contributing authors have declared a conflict of interest.

Availability of data and materials

All the necessary data will be provided upon request.

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.