BDNF Val66Met polymorphism and serum concentrations of BDNF with smoking in Thai males

Abstract

ABSTRACT. Many studies have suggested that brain-derived neurotrophic factor (BDNF) is involved in the reward system of addiction, and that nicotine may induce alterations in BDNF gene expression and its protein level within the mesocorticolimbic system. We investigated the BDNF levels and biochemical-hematological parameters of smoker and non-smoker groups, and examined the association of the Val66Met BDNF gene polymorphism with BDNF serum levels and cigarette smoking. The study sample comprised 311 Thai volunteers (200 smokers; 111 non-smokers). The levels of serum BDNF and biochemical-hematological parameters were determined. The Val66Met BDNF polymorphism was genotyped by the polymerase chain reaction-restriction fragment length polymorphism technique. The smoker group had significantly higher serum BDNF levels than the non-smoker group (8.3 vs 6.5 ng/mL, P < 0.05). BDNF concentrations correlated positively with hemoglobin, hematocrit, red blood cell count, white blood cell count, platelet count, number of cigarettes smoked, and thiocyanate level (P < 0.05). No association was found between the BDNF Val66Met genotype and the serum BDNF level. The BDNF Val66Met polymorphism was not significantly associated with the smoking status of the Thai males in this study. Cigarette smoking may be one factor that determines the serum BDNF level, but the BDNF Val66Met polymorphism probably does not influence susceptibility to smoking among Thai males.

Meta-analytic method reveal a significant association of theBDNF Val66Met variant with smoking persistence based on a large samples

“…Consistently, multiple lines of evidence have documented that the genetic variant of rs6265 is significantly associated with various psychiatric diseases, including schizophrenia, bipolar, and eating disorders [53,54]. Furthermore, a number of genetic researches have reported a potential association between the common Val66Met variant and susceptibility to smoking-related phenotypes [23,[35][36][37][38][39][40][41][42]. For example, a large-scale GWAS [19] identified the polymorphism of rs6265 was significantly associated with smoking initiation (OR = 1.06, 95% CI 1.08-1.18, P = 3.6 × 10 −8 ).…”

“…According to the "Quality of Reporting of meta-analysis and PRISMA guidelines" [43], nine studies [23,[35][36][37][38][39][40][41][42] were read carefully for potent eligible dataset according to a strictly systematic and comprehensive review (see Supplementary Fig. S1 for details).…”

“…The functional polymorphism of Val66Met was observed to change BDNF intracellular packaging and trafficking, which affects the activity-dependent secretion of BDNF protein [33]. Since Beuten et al first [34] found a significant link between genetic variant in BDNF and dependence of nicotine in male smokers based on European-American origin, a growing number of geneticsbased association researches [23,[35][36][37][38][39][40][41][42] have been performed to reveal the genetic correlation of rs6265 with cigarette smoking-related traits. Nevertheless, these results are still equivocal.…”

Neuroprotective Effects of Nicotine on Hippocampal Long-Term Potentiation in Brain Disorders

“…Most studies have provided strong evidence showing that exposure to nicotine leads to increased brain BDNF levels (Zhang et al, 2010;Suriyaprom et al, 2013;Jamal et al, 2015;Neves et al, 2017; for review, see Machaalani and Chen, 2018). The expression of BDNF and its tyrosine kinase receptor B receptor are linked to a7nAChRs where evidence shows BDNF and nAChRs mutually influencing each other (Freedman et al, 1993;.…”

Brain-Derived Neurotropic Factor Val66Met Polymorphism and Posttraumatic Stress Disorder among Survivors of the 1998 Dongting Lake Flood in China

“…Specifically, BDNF serum levels were lower in Met carriers than in Val/Val homozygotes [27, 28]. On the contrary, some studies found no association between this variant and BDNF serum levels [57, 58], while others found decreased BDNF serum levels in healthy Val/Val homozygotes when compared to Val/Met heterozygotes [59]. These inconsistent results across studies may be explained by a great variation in sample characteristics, assessment methods, and sample sizes.…”