Our search for genes influencing AUD development first looked for genetic linkage in mice, and we discovered 13 candidate QTL contributing to ethanol-induced ataxia. These hypothetical QTL were examined for genetic associations with alcohol-induced ataxia in humans. With candidate loci as a hypothesis, we reduced the number of statistical tests in comparison with a genome-wide association approach and thus increased the statistical power to detect genetic associations at the human loci. We also obtained greater genetic resolution and human relevance.
