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<p>The genetic mechanisms underlying tardive dyskinesia (TD) are crucial for understanding its development. This study aimed to examine the association between single nucleotide polymorphisms (SNPs) in the Glutamate Ionotropic Receptor NMDA Type Subunit (<i>GRIN2A</i>) and Cholinergic Receptor Muscarinic 2 (<i>CHRM2</i>) genes and their interactions with the susceptibility, severity of symptoms, and cognitive function of TD in Chinese Han patients with schizophrenia (SZ). A total of 216 SZ patients were categorized into TD and those without TD (WTD) groups. DNA was extracted using the high-salt method, and the SNP genotyping was conducted. TD severity was assessed using the Abnormal Involuntary Movement Scale (AIMS), while cognitive function was measured with the Repetitive Battery for the Assessment of Neuropsychological Status (RBANS). The <i>GRIN2A</i> rs7206256 GG + GA genotypes showed significantly different frequencies compared to the AA genotype (OR = 0.32, 95% CI = 0.13–0.79, <i>p</i> = 0.007). TD patients with the rs7206256 GG genotype exhibited higher limb trunk scores (<i>p</i> &lt; 0.01), and lower orofacial scores (<i>p</i> &lt; 0.01). Additionally, significant differences in attention and total RBANS scores were observed across <i>CHRM2</i> rs2061174 genotypes within the TD group (F = 2.55, <i>p</i> = 0.05; F = 5.08, <i>p</i> = 0.05). The combination of <i>CHRM2</i> (rs1824024)-<i>GRIN2A</i> (rs7206256) and <i>CHRM2</i> (rs2061174)-<i>GRIN2A</i> (rs7206256) were identified as the best two-SNP model for predicting TD risk (<i>p</i> = 0.05). In Chinese Han SZ patients, <i>GRIN2A</i> rs7206256 is associated with increased susceptibility to TD and greater symptom severity. <i>CHRM2</i> rs2061174 might influence cognitive dysfunction in TD, and a potential gene-gene interaction between <i>GRIN2A</i> and <i>CHRM2</i> loci was observed. These findings need confirmation through larger, multi-center studies with diverse populations and functional genomic analyses to uncover the biological mechanisms involved.</p>

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CHRM2 and GRIN2A polymorphisms in tardive dyskinesia and cognitive impairments in Chinese Han schizophrenia

  • 期刊论文

  • 发表日期：

    2025年5月30日

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  • Chenghao Lu,
  • Linxuan Wang,
  • Jing Wang,
  • Min Zeng,
  • Xiao Zhang,
  • Yanzhe Li,
  • Xiaofei Zhang,
  • Nannan Liu,
  • Jinghui Chi,
  • Lili Wang,
  • Shen Li

摘要

The genetic mechanisms underlying tardive dyskinesia (TD) are crucial for understanding its development. This study aimed to examine the association between single nucleotide polymorphisms (SNPs) in the Glutamate Ionotropic Receptor NMDA Type Subunit (GRIN2A) and Cholinergic Receptor Muscarinic 2 (CHRM2) genes and their interactions with the susceptibility, severity of symptoms, and cognitive function of TD in Chinese Han patients with schizophrenia (SZ). A total of 216 SZ patients were categorized into TD and those without TD (WTD) groups. DNA was extracted using the high-salt method, and the SNP genotyping was conducted. TD severity was assessed using the Abnormal Involuntary Movement Scale (AIMS), while cognitive function was measured with the Repetitive Battery for the Assessment of Neuropsychological Status (RBANS). The GRIN2A rs7206256 GG + GA genotypes showed significantly different frequencies compared to the AA genotype (OR = 0.32, 95% CI = 0.13–0.79, p = 0.007). TD patients with the rs7206256 GG genotype exhibited higher limb trunk scores (p < 0.01), and lower orofacial scores (p < 0.01). Additionally, significant differences in attention and total RBANS scores were observed across CHRM2 rs2061174 genotypes within the TD group (F = 2.55, p = 0.05; F = 5.08, p = 0.05). The combination of CHRM2 (rs1824024)-GRIN2A (rs7206256) and CHRM2 (rs2061174)-GRIN2A (rs7206256) were identified as the best two-SNP model for predicting TD risk (p = 0.05). In Chinese Han SZ patients, GRIN2A rs7206256 is associated with increased susceptibility to TD and greater symptom severity. CHRM2 rs2061174 might influence cognitive dysfunction in TD, and a potential gene-gene interaction between GRIN2A and CHRM2 loci was observed. These findings need confirmation through larger, multi-center studies with diverse populations and functional genomic analyses to uncover the biological mechanisms involved.