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.
Based on the literature, we hypothesized that the 5-HT2A and 5-HT2C receptor polymorphisms would be associated with agitation/aggression and psychosis and the 5-HTTPR or 5-HTTVNTR polymorphisms, with agitation/aggression or depression and anxiety.
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 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.
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.
Our results showed that the distribution of the BDNFVal66Met genotype in Chinese subjects with methamphetamine dependence (OR=2.6, p=0.015) and methamphetamine psychosis (OR=0.2, p = 0.034) were significant compared with controls.
Preliminary evidence suggests that polymorphisms within the catechol-O-methyltransferase and brain-derived neurotrophic factor genes may interact with psychosocial stress in the development of psychosis; however, extensive further investigations are required to confirm this.
There was no genetic association between HTR2AT102C with either schizophrenia or bipolar disorder under the assumption of a parent-of-origin effect, and these data together essentially exclude imprinting at this locus as a potential explanation for the complex inheritance observed in major psychoses.
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.
Subjects with possible or probable AD or mild cognitive impairment (MCI) without psychosis at study entry were genotyped for the HTR2AT102C polymorphism and reassessed every 6 months until psychosis onset.
In this review we primarily focus on psychosis in PD, the current treatment possibilities and the new, emerging therapy, pimavanserin, a selective 5-HT2A inverse agonist.