miR-7 and miR-153 have both been recently implicated in the regulation of α-synuclein (Doxakis, 2010). α-synuclein plays a role in activity-dependent maintenance of SNARE complex levels in pre-synaptic terminals (Burre et al., 2010; Greten-Harrison and Polydoro, 2010; Burgoyne and Morgan, 2011) and is involved in dopaminergic neurotransmission and neurodegenerative disorders (Doxakis, 2010). Importantly, there is a large body of evidence linking α-synuclein accumulation to alcohol dependency in humans as well as in rodents (Bönsch et al., 2005; Liang and Carr, 2006; Foroud et al., 2007; Taraskina et al., 2008; Aho et al., 2009). Furthermore, miR-7 has also been implicated in the control of neurite outgrowth in vitro, during neuronal differentiation of human neuroblastoma cell lines (Chen et al., 2010). On the other hand, miR-153 has been implicated in the teratogenic effects of alcohol in mice, although in this case, due to downregulation of the combinatorial function of three miRNAs (miR-21, miR-335, and miR-153). Simultaneous downregulation of these three miRNAs allowed their shared target, Jagged1 (a Notch receptor ligand), to accumulate and induce cell cycle and neuroepithelial maturation (Sathyan et al., 2007).
