Abstract
BACKGROUND: Post-stroke depression (PSD) is a common neuropsychiatric complication after a stroke with complex mechanisms. However, few studies have identified the role of vitamin B12 and folate in the occurrence and pathophysiology of PSD. The aim of our study is to investigate the relationship among vitamin B12, folate, their transporter genes, and early-onset PSD. METHOD AND MATERIAL: A total of 173 ischemic stroke patients were recruited in Xiangya Hospital of Central South University. We collected peripheral blood samples, clinical data, and demographics at admission. The 17-item Hamilton Depression Scale was used for screening for the existence of depression at 2 weeks after stroke onset. Serum vitamin B12 and folate level were measured based on double-antibody sandwich enzyme-linked immune-sorbent assay. Four single nucleotide polymorphisms (SNP) of transcobalamin 2 (TCN2) and solute carrier family 19 member 1 were genotyped using SNPscan(TM) multiplex SNP typing Kit. RESULTS: Eighty-four patients were diagnosed with PSD at 2 weeks after stroke onset, and the incidence rate was 48.6%. Serum vitamin B12 level in PSD group was significantly lower than those in the non-PSD group (p=0.018). Binary logistic regression revealed that TCN2 rs1801198 GG genotype and G allele were associated with an increased risk of PSD after adjustment for confounding factors (for GG genotype, OR = 4.253, 95% CI = 1.711~10.572, p = 0.002; for G allele, OR = 2.134, 95% CI = 1.362~3.343, p = 0.001). Moreover, individuals with the rs1801198 G allele in the PSD group exhibited lower vitamin B12 level than those with the rs1801198 G allele in the non-PSD group (p=0.045). CONCLUSION: TCN2 rs1801198 and vitamin B12 are associated with the risk of early-onset PSD, and they may be involved in the development of PSD. Our study presents a novel standpoint for the treatment of PSD and gains insights into the mechanistic underpinnings of PSD.