Genetic variation in hyperpolarization-activated cyclic nucleotide-gated channels and its relationship with neuroticism, cognition and risk of depression

Andrew M. McIntosh, Arthur A. Simen, Kathryn L. Evans, Jeremy Hall, Donald J. MacIntyre, Douglas Blackwood, Andrew D. Morris, Blair H. Smith, Anna Dominiczak, David Porteous, Ian J. Deary, Pippa A. Thomson

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    Abstract

    Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are encoded by four genes (HCN1-4) and, through activation by cyclic AMP (cAMP), represent a point of convergence for several psychosis risk genes. On the basis of positive preliminary data, we sought to test whether genetic variation in HCN1-4 conferred risk of depression or cognitive impairment in the Generation Scotland: Scottish Family Health Study. HCN1, HCN2, HCN3, and HCN4 were genotyped for 43 haplotype-tagging SNPs and tested for association with DSM-IV depression, neuroticism, and a battery of cognitive tests assessing cognitive ability, memory, verbal fluency, and psychomotor performance. No association was found between any HCN channel gene SNP and risk of depression, neuroticism, or on any cognitive measure. The current study does not support a genetic role for HCN channels in conferring risk of depression or cognitive impairment in individuals from the Scottish population.
    Original languageEnglish
    Article number00116
    JournalFrontiers in Genetics
    Volume3
    Early online date2 Jul 2012
    DOIs
    Publication statusPublished - 2012

    Keywords

    • Stress
    • Depression
    • HCN channel
    • Genetics
    • Association
    • Cognition
    • Neuroticism

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    McIntosh, A. M., Simen, A. A., Evans, K. L., Hall, J., MacIntyre, D. J., Blackwood, D., Morris, A. D., Smith, B. H., Dominiczak, A., Porteous, D., Deary, I. J., & Thomson, P. A. (2012). Genetic variation in hyperpolarization-activated cyclic nucleotide-gated channels and its relationship with neuroticism, cognition and risk of depression. Frontiers in Genetics, 3, [00116]. https://doi.org/10.3389/fgene.2012.00116