Brain-derived neurotrophic factor (BDNF) is a biomarker for neuroplasticity-related mechanisms compromised in depression and recovered by conventional antidepressants, including synaptic plasticity, cell survival, neurogenesis and spine formation.
Brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) levels in post-mortem brain tissue from patients with depression compared to healthy individuals - a proof of concept study.
Brain-derived neurotrophic factor (BDNF) has appeared to play a critical role in certain neurobiological modifications that may otherwise lead to schizophrenia or depression.
A brain-derived neurotrophic factor (BDNF) prodomain single-nucleotide polymorphism resulting in a valine to methionine substitution (Val66Met) has been associated with depression-related phenotypes and brain alterations involving regions consistently associated with major depressive disorder (MDD).
A conserved BDNF, glutamate- and GABA-enriched gene module related to human depression identified by coexpression meta-analysis and DNA variant genome-wide association studies.
A decrease in BDNF was observed in CS vs controls (P = 0.038), and low BDNF was associated with more anxiety (r = -0.247, P = 0.037), depression (r = -0.249, P = 0.035), stress (r = -0.277, P = 0.019) and affective balance (r = 0.243, P = 0.04).
A functional BDNF polymorphism (BDNFVal66Met) was reported to influence the effects of stressful life events or childhood adversity on depression and suicidal behaviour in various psychopathologies.
A genetic variant (rs6265) of the brain-derived neurotrophic factor (BDNF) impacting on emotion processing is known to increase the risk for depression.
A great research effort is devoted to identify the molecular mechanisms that are responsible for the network effects of depression and antidepressant actions, with a great deal of evidence pointing at a key role of neurotrophins (notably the brain-derived neurotrophic factor) and other growth factors.
A logistic regression model investigating age, sex, serum BDNF levels, dietary quality and depression, as well as any interactions, found that lower dietary quality, and surprisingly, higher BDNF levels, were associated with increased depression risk, P = 0.037 and P < 0.001, respectively.
A mediation approach ((G × G) × E mediation model) was employed to confirm the indirect effects of ELS on the relationship between 5-HTTPLR × BDNF polymorphism combinations and depression subtype.
A multivariable linear regression model showed that the best predictors of depression were the SF-36 General health (β = -0.209; P = 0.013), Mental health (β = -0.410; P < 0.001) and Social activity (β = -0.195; P = 0.035) scores; physical disability (assessed by the Extended Disability Status Scale score) was directly correlated to depression severity on univariate analysis, but it was not a relevant predictor of depression on multivariate analysis; other variables directly related to the disease (treatment, annual relapsing rate) and the BDNFVal66Met polymorphism were not significantly associated with depression.
A review of the literature is provided on the relationship between brain-derived neurotrophic factor and sex steroid hormones, as well as the mechanisms behind this interaction, in the context of how this relationship may be involved in the development of neurodevelopmental psychiatric illnesses, such as schizophrenia and depression.
A single nucleotide polymorphism in the human BDNF gene (Val66Met) affects memory, and influences Alzheimer's disease and depression vulnerability in a sex-specific manner.
A single-nucleotide polymorphism in the BDNF gene (BDNFVal66Met), associated with depression and anxiety, has been proposed as a genetic risk factor for CVD.