SLC18A2 shuttles cytosolic monoamines into synaptic vesicles. Schwab and colleagues (2005) reported an association with variation in SLC18A2 (10q25) and AD, but we are unaware of any reports of association with other disinhibitory psychopathology. SLC6A3 terminates DA signaling by removing this neurotransmitter from synaptic clefts. Some research has indicated that striatal SLC6A3 density and availability is reduced in alcohol-dependent subjects (Lind et al., 2009). van der Zwaluw and colleagues’ (2009) review notes that many investigators have identified association between SLC6A3's (5p15.3) best studied 40-bp VNTR and alcohol-withdrawal symptoms but typically not with AD. Generally, association studies of other drug use phenotypes and SLC6A3 have been negative (Bousman et al., 2009; Li et al., 2006), although Guindalini and colleagues (2006) did find that alleles in a 30-bp VNTR increased risk of cocaine abuse. Additionally, there have been mixed results of association with SLC6A3's functional 40-bp VNTR in relation to antisocial behavior in adolescence (Burt and Mikolajewski, 2008; Guo et al., 2007; Jorm et al., 2001; Schulz-Heik et al., 2008; Young et al., 2002). The meta-analysis of Gizer and colleagues (2009) found association of variants in SLC6A3 with ADHD.
