Abstract
Tourette syndrome (TS) is a polygenic neuropsychiatric disease. Previous studies have indicated that dysregulation in the histaminergic system may play a crucial role in disease onset. In this study, we investigated the role of the histidine decarboxylase gene (HDC) in TS susceptibility in the Chinese Han population. After genotyping 241 TS nuclear families trios, we analyzed three tag HDC single nucleotide polymorphisms (rs854150, rs854151, and rs854157) in a family-based study using the transmission disequilibrium test (TDT) and haplotype relative risk (HRR). TDT showed no over-transmission in these SNPs across the HDC region (for rs854150: χ2 = 0.472, P = 0.537, OR = 1.097, 95%CI = 0.738–1.630; for rs854151: χ2 = 0.043, P = 0.889, OR = 1.145, 95%CI = 0.767–1.709; for rs854157:χ2 = 0.984, P = 0.367, OR = 1.020, 95%CI = 0.508–2.049). HRR also showed the same tendency (for rs854150: χ2 = 0.211, P = 0.646, OR = 1.088, 95%CI = 0.759–1.559; for rs854151: χ2 = 0.134, P = 0.714, OR = 0.935, 95%CI = 0.653–1.339; for rs854157:χ2 = 0.841, P = 0.359, OR = 1.206, 95%CI = 0.808–1.799). Additionally, the haplotype-based haplotype relative risk showed a negative association. Although these findings indicate an unlikely association between HDC and TS in the Chinese Han population, a potential role for HDC cannot be ruled out in TS etiology. Future research should investigate this more thoroughly using different populations and larger samples.
Highlights
Tourette syndrome (TS) is a neuropsychiatric disease presenting as multiple motor and vocal tics that begin during childhood
TS is a complex neuropsychiatric illness resulting from an interaction between genetics, the environment, immunology, and hormonal factors[13]
Ercan-Sencicek et al recently detected a rare mutation in a TS family in which the father and eight of his children were affected with the disease [7]
Summary
Tourette syndrome (TS) is a neuropsychiatric disease presenting as multiple motor and vocal tics that begin during childhood. The disorders originating from TS sometimes lessen with age, the co-morbid symptoms may continue until adolescence and even adulthood [2,3]. The occurrence of multiple conditions may present a challenge to the complicated pathogenesis of TS. Studies of candidate genes have typically focused on neurotransmitters and neuromodulators, and dopaminergic neurotransmission, with dopamine receptors D1–D4 and dopamine β–hydroxylase often deemed causative loci of TS [6]. W317X,c.951G>A) in the histidine decarboxylase gene (HDC) in a two-generation pedigree of a family with a high incidence of TS [7];this indicates a role for histaminergic neurotransmission in the onset and development of TS
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