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Chronic alcohol consumption is characterized by disturbances of neuroplasticity. Brain-derived neurotrophic factor (BDNF) is believed to be critically involved in this process. Here we aimed to review actual experimental and clinical data related to BDNF participation in neuroplasticity in the context of alcohol dependence. As has been shown in experiments with rodents, alcohol consumption is accompanied by the brain region-specific changes of BDNF expression and by structural and behavioral impairments. BDNF reverses aberrant neuroplasticity observed during alcohol intoxication. According to the clinical data parameters associated with BDNF demonstrate close correlation with neuroplastic changes accompanying alcohol dependence. In particular, the rs6265 polymorphism within the BDNF gene is associated with macrostructural changes in the brain, while peripheral BDNF concentration may be associated with anxiety, depression, and cognitive impairment. Thus, BDNF is involved in the mechanisms of alcohol-induced changes of neuroplasticity, and polymorphisms within the BDNF gene and peripheral BDNF concentration may serve as biomarkers, diagnostic or prognostic factors in treatment of alcohol abuse.

Brain-derived neurotrophic factor (BDNF) functions not only in the brain but also in peripheral tissues such as the liver. Genetic factors determine the development of alcohol dependence and somatic consequences of chronic intoxication, especially liver cirrhosis. The BDNF gene polymorphisms are associated with alcohol dependence; however, their relationship with the development of alcohol-related liver cirrhosis (ALC) has not yet been established. This study evaluated the association between single-nucleotide polymorphisms (SNPs) within the BDNF gene and liver cirrhosis in heavy drinkers. BDNF-related SNPs rs925946, rs6265, rs10835210, rs7103411, and rs75945125 were determined using real-time PCR in heavy drinkers with and without liver cirrhosis. Single SNPs and defined haplotypes within the BDNF gene were tested for association with ALC. According to both codominant and recessive genetic models, carriers of the rs925946 TT genotype have an elevated risk of liver cirrhosis development with odds ratios (confidence intervals) 6.287 (1.286-30.738) and 6.321 (1.317-30.348), respectively. BDNF SNPs rs6265, rs10835210, rs7103411, and rs75945125 do not associate with risk of ALC. One block of haplotypes consisting of rs10835210 and rs7103411 demonstrated linkage disequilibrium (D' = 1 and r.sup.2 = 0.228). The revealed haplotypes do not associate with the development of liver cirrhosis in alcohol heavy drinkers. Thus, the BDNF rs925946 SNP is associated with the risk of ALC in heavy drinkers. Future investigations of the BDNF gene-related genetic markers of ALC will help to objectively assess the risk and severity of liver damage and correct the corresponding therapy.