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.
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.
High serum levels of BDNF and glutamate were associated with response to clozapine, while glutamate levels correlated with the psychosis severity in clozapine responders only.
We aimed to investigate whether there is a gene-environment interaction in the relationship between stress and BDNFVal66Met polymorphism in relation to dietary patterns in a sample of subjects with early psychosis.
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.
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.
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.
Further, our study supports a two hit model including a history of childhood trauma as well as genetic vulnerability (met carriers of the BDNFval66met) behind reduced volume of hippocampal subfields in psychosis.
The three-way pICA approach identified links between a SNP component (pointing to brain function and mental disorder associated genes, including BDNF, GRIN2B and NRG1), a functional component related to increased activation in the precuneus area, and a gray matter component comprising part of the default mode network and the caudate.
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.
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.
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.
The current, limited evidence points to genes that are not specifically involved in psychosis but more generally in regulating mood (serotonin transporter gene), neuroplasticity (brain-derived neurotrophic factor), and the stress-response system (FKBP5), in line with a general effect of CT on a range of mental disorders, rather than suggesting specificity for psychosis.
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.