In this study, we examined whether brain-derived neurotrophic factor (BDNF) and its receptor TrkB signaling plays a role in the risk for psychosis after exposure of cannabinoid (CB) receptor agonist during adolescence.
These findings provide evidence of the important role of early cannabis use and the Val66MetBDNF polymorphism on age at psychosis onset and they point out to sex-specific differences in cannabis use patterns.
Finally, we observe that frontal-cortex DNA methylation in the BDNF gene is correlated with genotype at a nearby nonsynonymous SNP that has been previously associated with major psychosis.
To begin to address this issue, we conducted high-coverage targeted exome capture in a subset of neurotrophin genes in 48 comprehensively characterized cases with schizophrenia-related psychosis.
Brain derived neurotrophic factor (BDNF) is important for brain development and plasticity, and here we tested if the functional BDNFval66met variant modulates the association between high levels of childhood abuse, cognitive function, and brain abnormalities in psychoses.
There was no difference in the proportion of Met allele carriers between FEP patients and controls, and no significant influence of BDNF genotype on cognitive test scores in either of the psychosis groups.
This study aimed to investigate the degree of DNA methylation at the promoter region of the brain-derived neurotrophic factor (BDNF) gene, as one of the candidate genes associated with major psychoses, in peripheral blood mononuclear cells isolated from 94 patients with BD (BD I=49, BD II=45) and 52 healthy controls.
The present study aimed to explore possible effects of BDNFVal66Met polymorphism variations on progressive structural brain changes after 3 years from the first episode of psychosis.
In this first phase of the project, the objective was to investigate the distribution of four candidate genetic polymorphisms for functional psychosis (Ser9Gly DRD3, 5HTTLPR, the VNTR 3'-UTR SLC6A3 and Val66MetBDNF) in a case-control sample.
The results had adequate statistical power to suggest that BDNFVal66Met was not related to susceptibility to AD or the onset of AD, but that presence of one or two Met alleles of BDNFVal66Met polymorphism might present a risk factor for psychosis in AD.
A larger sample size, and evaluation of more single-nucleotide polymorphisms are needed to obtain more robust and conclusive findings regarding the relationship between the BDNF gene and psychosis.
A complex interplay between BDNF serum concentrations, personality traits, BDNFVal66Met polymorphism, and psychotic symptomatology has been arisen but further investigation is needed to better clarify the observed associations.
Multiple regression analysis revealed a significant positive association of plasma BDNF levels with planning ability across all groups.<b>Conclusions:</b> The lower peripheral BDNF levels in ARMS compared to FEP and CS might point towards an important drop of this neurotrophin prior to the onset of frank psychosis.
However, baseline levels of serum BDNF did not predict the development of psychosis (OR=0.64, CI = 0.40 - 1.02) or remission (OR=0.83, CI = 0.60 - 1.15) from UHR status.