influencing risk for AD mapping in the vicinity of an alcohol dehydrogenase (ADH) gene cluster on chromosome 4q (see below). Several other linkage peaks, even those that did not meet standard criteria for genomewide significance, have led to the identification of likely disease-influencing loci. In addition, Wilhelmsen et al. (2003) reported a genomewide linkage study for the trait of low-level response to alcohol, which has been shown prospectively to increase risk for the development of AD (Schuckit 2009). Although this study involved a relatively small sample (139 sibling pairs chosen from among non-alcohol-dependent students attending two universities in San Diego, CA), several “suggestive” linkages were identified. Ehlers et al. (2004), in a linkage analysis using 791 microsatellite markers in 243 Mission Indians in the southwest United States, found several lod scores in excess of 2.0 for the phenotypes of alcohol severity (chromosomes 4 and 12) and alcohol withdrawal (chromosomes 6, 15, and 16). More recently, Prescott et al. (2006) reported on linkage analysis in a set of 474 small families recruited in Ireland. The strongest results from this study (up to a multipoint lod score of 4.59) were also on chromosome 4. In the only genomewide linkage study of AD
