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.
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.
While the hypo-activity of serotonin signaling is involved in the pathogenesis of depression, anxiety and obsessive compulsive disorder; LSD, an agonist of serotonin type 2 receptor (5-HTR2A) induces psychosis.
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.
The brain-derived neurotrophic factor (BDNF) is a key regulator of synaptic plasticity and has been suggested to be involved in the pathophysiology and pathogenesis of psychotic disorders, with particular emphasis on dysfunctions of the hippocampus.
HTR2A gene has been the subject of numerous studies in psychiatric genetics because LSD, which resembles serotonin causes psychosis and atypical antipsychotic drugs target the HTR2A receptor.
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.
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.