Journal of affective disorders · 2026
Differential analysis of CACNA1C polymorphisms among patients with depression and bipolar disorder and exploration of sleep as a mediator.
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Xu Zhi, Guo Yang, Shao Yongqi, Shen Tian, Chen Lei, Chen Zimu, Chen Suzhen, Chen Bingwei, Yuan Yonggui, Cai Yang
Аннотация
BACKGROUND: Differentiating the depressive phase of bipolar disorder (BD) from major depressive disorder (MDD) remains a significant clinical challenge. As CACNA1C is a prominent susceptibility gene for BD across diverse populations, this study evaluated the utility of its polymorphisms, combined with clinical risk factors, in distinguishing BD from MDD, while investigating the potential mediating role of sleep quality.
METHODS: Subjects (188 MDD, 69 BD) were compared using Mann-Whitney U or chi-square tests. Logistic regression identified independent discriminative factors. Forty-two CACNA1C SNPs were analyzed via Haploview and UNPHASED to assess genetic distributions. Mediation analysis evaluated whether sleep quality mediates the relationship between CACNA1C variants and the BD phenotype.
RESULTS: Younger onset age, positive family history, and psychotic symptoms were independently associated with BD diagnosis. Genetically, SNP rs2239128 showed a significant association with BD (adjusted P = 0.04895). Moderate linkage disequilibrium (LD) was observed for rs215976/rs215992 (r2 = 0.543, D' = 0.801), and weak LD for rs215995/rs123263 (r2 = 0.157, D' = 0.433). Four haplotypes-rs215976/rs215992 CC (OR = 0.257) and rs215995/rs123263 T-G (OR = 0.112), C-T (OR = 0.029), and C-G (OR = 0.814)-were significantly associated with BD (all P < 0.05). Sleep quality showed no significant mediating effect.
CONCLUSION: Integrated clinical risk factors and CACNA1C genetic variations are promising indicators for differentiating BD from MDD. Although sleep quality did not demonstrate a mediating role, these findings contribute preliminary insights into the distinct genetic and phenotypic architecture of these disorders, offering a foundation for future mechanistic exploration and personalized interventions.
METHODS: Subjects (188 MDD, 69 BD) were compared using Mann-Whitney U or chi-square tests. Logistic regression identified independent discriminative factors. Forty-two CACNA1C SNPs were analyzed via Haploview and UNPHASED to assess genetic distributions. Mediation analysis evaluated whether sleep quality mediates the relationship between CACNA1C variants and the BD phenotype.
RESULTS: Younger onset age, positive family history, and psychotic symptoms were independently associated with BD diagnosis. Genetically, SNP rs2239128 showed a significant association with BD (adjusted P = 0.04895). Moderate linkage disequilibrium (LD) was observed for rs215976/rs215992 (r2 = 0.543, D' = 0.801), and weak LD for rs215995/rs123263 (r2 = 0.157, D' = 0.433). Four haplotypes-rs215976/rs215992 CC (OR = 0.257) and rs215995/rs123263 T-G (OR = 0.112), C-T (OR = 0.029), and C-G (OR = 0.814)-were significantly associated with BD (all P < 0.05). Sleep quality showed no significant mediating effect.
CONCLUSION: Integrated clinical risk factors and CACNA1C genetic variations are promising indicators for differentiating BD from MDD. Although sleep quality did not demonstrate a mediating role, these findings contribute preliminary insights into the distinct genetic and phenotypic architecture of these disorders, offering a foundation for future mechanistic exploration and personalized interventions.