Brain-derived neurotrophic factor (BDNF) has been implicated in the pathogenesis of mood disorders, and the aim of the present study was to test for the presence of linkage disequilibrium between two polymorphisms in the BDNF gene and BP in 283 nuclear families.
Based on several lines of evidence, BDNF has been hypothesized to play an important role in the pathogenesis of mood disorder and the therapeutic action of at least some effective treatments.
Several lines of evidence suggest that a certain type of personality or temperament is at risk for developing neuropsychiatric diseases, and that brain-derived neurotrophic factor (BDNF) might be involved in pathophysiology of neuropsychiatric diseases such as mood disorders.
Our results suggest that mood disorder is associated with PKA upregulation and this could mask alteration in BDNF expression, because slowing down of PKA signaling results in a decrease of BDNF expression.
Variations in two single-nucleotide polymorphisms (SNPs) within the BDNF gene have previously been associated with AD, and one of these SNPs has also been associated with memory loss and affective disorders.
Genetic variation at the locus encoding the brain derived neurotrophic factor (BDNF) has been implicated in some neuropsychiatric disorders such as Alzheimer's disease (AD), affective disorders (AFDs), schizophrenia, and substance dependence.
In the present study we investigated the influence of a series variants in genes (the serotonin transporter, glycogen synthase kinase-3beta, inositol polyphosphatase 1-phosphate, brain-derived neurotrophic factor and activator protein 2beta) related to the action of lithium carbonate, a drug used for prophylaxis in mood disorders.
We review pertinent data on BDNF from several different areas of preclinical and clinical investigation that suggest novel theoretical and treatment implications for the recurrent affective disorders.
In the present study, we evaluated the impact of the BDNFVal66Met polymorphism on individual differences in personality traits in a sample of healthy volunteers in relation to other common gene variants thought to be involved in the pathophysiology of affective disorders, such as the serotonin transporter promoter polymorphism (5-HTTLPR) and a variable number of tandem repeat polymorphism of the dopamine transporter gene (DAT VNTR).
Advances in BDNF cell biology, including its transcription through multiple promoters, trafficking and secretion, may provide new insights into its role in mood disorders.
The results for NTRK3 as well as the authors' previous finding for association to brain-derived neurotrophic factor in this sample support synaptic plasticity as a mechanism contributing to mood disorders that begin during childhood and adolescence and specifically implicate the NTRK3 gene as a contributing factor in the 15q-linked region.
Further investigations in larger samples are needed to clarify the usefulness of 5-HTTLPR and BDNFVal66Met genotyping in the optimization of non-pharmacological treatments in mood disorders.
Because intermediate phenotypes may help to identify genetic contributors to COMD, we tested for an association between variants in the brain-derived neurotrophic factor (BDNF) gene and theta EEG asymmetry, both of which have been independently implicated in affective disorders.
The observed structural abnormality in the brains of patients with mood disorders has been related to abnormal brain-derived neurotrophic factor (BDNF) function, suggesting an important role for BDNF in these disorders.