Abstract
Drug addiction is a term applied across substance use disorders (SUDs) and defined as a chronic, relapsing complex brain disease characterized by compulsive drug seeking, craving, loss of self-control, and impaired decision making (National Institute on Drug Abuse 2010). Drug addiction persists in spite of harmful consequences and cuts across all demographics. Addiction results from the interactive effects among multiple genes, acting in multiple environments, and across multiple stages of development. It is this intersection that roots SUDs, in concert with other biological processes, in genetic and epigenetic mechanisms that provide a scaffold for normal brain development, for learning and memory, and for pathophysiology.
Highlights
Drug addiction is a term applied across substance use disorders (SUDs) and defined as a chronic, relapsing complex brain disease characterized by compulsive drug seeking, craving, loss of self-control, and impaired decision making (National Institute on Drug Abuse 2010)
Genetic research on SUDs has transitioned from candidate gene and linkage methods to genome-wide association studies (GWAS) and sequencing-based approaches
Many studies have been fruitful mainly because studying the genetics of SUDs benefits from a vast knowledge of a given drug’s mechanism of action (Rutter 2006). Among these are genes encoding for the enzymes involved with drug metabolism such as alcohol and aldehyde dehydrogenases, which offer protection against alcoholism (Chen et al 2009) and CYP2A6, which offers protections against nicotine addiction (Malaiyandi et al 2005)
Summary
Studies have identified gene variants that modulate the response to the rewarding or aversive effects of drugs such as the nicotinic cholinergic receptor subunit gene (CHRNA5, a5) for nicotine (Fowler et al 2011) and the l-opioid receptor gene (ORPM1) for alcohol and opioids (Arias et al 2006). This GWAS finding was crucial for identifying the importance of the medial habenula (MHb) and the interpeduncular nucleus (IPN), brain regions that express high levels of the a5 subunit containing receptors (Changeux 2010), and which form a brain circuit that plays a role in the aversive effects of nicotine.
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