The role of SLITRK6 in the pathogenesis of Tourette syndrome: From the conclusion of a family-based study in the Chinese Han population.

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    • Source:
      Publisher: John Wiley & Sons Country of Publication: England NLM ID: 9815764 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1521-2254 (Electronic) Linking ISSN: 1099498X NLM ISO Abbreviation: J Gene Med Subsets: MEDLINE
    • Publication Information:
      Original Publication: Chichester, UK : John Wiley & Sons,
    • Subject Terms:
    • Abstract:
      Background: Tourette syndrome (TS) is a complex neuropsychiatric disorder coupled with obvious genetic heterogeneity. Studies in recent years have confirmed the association of SLITRK genes with sensory and neuropsychiatric diseases. To detect whether SLITRK6 is involved in the progress of TS, a family-based association study was performed to explore the possible genetic association between SLITRK6 and TS in the Chinese Han population.
      Methods: We genotyped 399 TS nuclear families trios, and then analyzed three tag SLITRK6 single nucleotide polymorphisms using the transmission disequilibrium test (TDT) haplotype relative risk (HRR) and haplotype-based haplotype relative risk (HHRR) methods.
      Results: The TDT showed no statistically significant allele transfer for the three polymorphisms. The HRR and HHRR also showed a negative association.
      Conclusions: Despite the results suggesting that these polymorphisms may not be associated with susceptibility to TS in the Chinese Han population, we are still unable to determine the potential role of SLITRK6 in the pathogenesis of TS. Furthermore, the results still need to be confirmed in a larger sample size and in different populations.
      (© 2020 John Wiley & Sons, Ltd.)
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    • Contributed Indexing:
      Keywords: SLITRK6 gene; Tourette syndrome; family-based association study; genetic susceptibility; single nucleotide polymorphisms
    • Accession Number:
      0 (Membrane Proteins)
      0 (Slitrk6 protein, human)
    • Publication Date:
      Date Created: 20200211 Date Completed: 20210715 Latest Revision: 20221207
    • Publication Date:
      20231215
    • Accession Number:
      10.1002/jgm.3173
    • Accession Number:
      32037697