Brain-derived neurotrophic factor (BDNF) is a major neurotrophin in the central nervous system that plays a critical role in the physiological brain functions via its two independent receptors: tropomyosin-related kinase B (TrkB) and p75, especially in the neurodevelopment. Disrupting of BDNF and its downstream signals has been found in many neuropsychological diseases, including attention-deficit hyperactivity disorder (ADHD), a common mental disorder which is prevalent in childhood. Understanding the physiological functions of BDNF during neural development and its potential relationship with ADHD will help us to elucidate the possible mechanisms of ADHD and to develop therapeutic approaches for this disease. In this review, we summarized the important literatures for the physiological functions of BDNF in the neurodevelopment. We also performed an association study on the functional genetic variation of BDNF and ADHD by a case-control study in the Chinese mainland population and revealed the potential correlation between BDNF and ADHD which needs further research to confirm.

Attention-deficit/hyperactivity disorder (ADHD) is a common and highly heritable childhood-onset psychiatric disorder with significant genetic contribution. Considerable evidence has implicated involvement of dopaminergic system and the prefrontal cortex (PFC) in the pathomechanism of ADHD. The catechol-O-methyltransferase (COMT) gene is of particular interest for ADHD as its crucial role in the degradation of dopamine in the PFC. We summarized the reported findings investigating associations between COMT gene and ADHD and performed a meta-analysis of previous studies to assess the overall magnitude and significance of the association.

Attention deficit/hyperactivity disorder (ADHD) is one of the most highly heritable psychiatric disorders in childhood. The risk gene mutation accounts for about 60 to 90 % cases. Synaptosomal-associated protein of 25 kDa (SNAP-25) is a presynaptic plasma membrane protein which is expressed highly and specifically in the neuronal cells. A number of evidences have suggested the role of SNAP-25 in the etiology of ADHD. Notably, the animal model of coloboma mouse mutant bears a ∼2-cM deletion encompassing genes including SNAP25 and displays spontaneous hyperkinetic behavior. Previous investigators have reported association between SNPs in SNAP25 and ADHD, and controversial results were observed. In this study, we analyzed the possible association between six polymorphisms (rs3746544, rs363006, rs1051312, rs8636, rs362549, and rs362998) of SNAP25 and ADHD in a pooled sample of ten family-based studies and four case-control studies by using meta-analysis. The combined analysis results were significant only for rs3746544 (P = 0.010) with mild association (odds ratio (OR) = 1.14). And, the meta-analysis data for rs8636, rs362549, and rs362998 are the first time to be reported; however, no positive association was detected. In conclusion, we report some evidence supporting the association of SNAP25 to ADHD. Future research should emphasize genome-wide association studies in more specific subgroups and larger independent samples.

BackgroundCoronary artery disease (CAD) is a leading cause of mortality in many countries. Considerable studies have been carried out to investigate the relationship between the C242T and A640G polymorphisms of CYBA gene and CAD, but the results were still inconsistent. Hence we conducted a meta-analysis to clarify the association.Methods and ResultsA total of 21 eligible literatures were included in the meta-analysis. We observed a significant decreased risk of CAD for C242T polymorphism in Asian population under an allelic model (OR 0.75; 95% CI 0.67–0.84) and a dominant model (OR 0.69; 95% CI 0.61–0.79), however, in overall population and other population no significant association was revealed. We also found A640G polymorphism may contribute to reducing CAD risk under an allelic model (OR 0.84; 95% CI 0.75–0.93), dominant model (OR0.77; 95% CI 0.64–0.92) and recessive model (OR0.82; 95% CI 0.69–0.97). No publication bias was found.ConclusionOur meta-analysis confirmed a protective effect of C242Tpolymorphism on CAD in Asian population and indicated that A640G polymorphism was significantly associated with decreased risk of CAD.

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