| Literature DB >> 22903349 |
Abstract
Alcohol dependence is caused by complex interactions of multiple susceptibility genes with little effect each and environmental factors. Candidate genes influence metabolism of alcohol, such as alcohol dehydrogenase and aldehyde dehydrogenase, and modulatory transmitter systems, such as the dopaminergic, serotonergic, acetylcholinergic, gamma-aminobutyric acidergic, and various neuropeptidergic systems. Dysfunctional behavioral choices, learning, and memory are involved in the etiology of alcohol dependence. Systematic promotion and maintenance of motivation is a lifetime challenge in the treatment of alcohol use disorders. The second step of treatment management is the discontinuation of alcohol consumption. Withdrawal symptoms can be treated with gamma-aminobutyric acidergic substances such as benzodiazepines. Long-term relapse prevention is another challenge. Multimodal treatment can include naltrexone, a non-selective opioid receptor antagonist, or acamprosate, an N-methyl-D-aspartate receptor modulator, which are first line for pharmacological treatment on the basis of recent Cochrane analyses. Due to the complexity of etiology with both psychological and neurobiological factors, future treatment management of alcoholism may include the combination of individualized disorder-specific psychotherapy and drugs acting on different neuronal pathways, on the basis of individual vulnerability. However, the question remains unsolved whether an individualized approach is feasible and how subgroups should be defined.Entities:
Mesh:
Year: 2012 PMID: 22903349 DOI: 10.1007/s00702-012-0886-8
Source DB: PubMed Journal: J Neural Transm (Vienna) ISSN: 0300-9564 Impact factor: 3.575