Clinical and preclinical studies have demonstrated that depression, one of the most common psychiatric illnesses, is associated with reduced levels of neurotrophic factors, including brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF), contributing to neuronal atrophy in the prefrontal cortex (PFC) and hippocampus, and reduced hippocampal adult neurogenesis.
The proposed model is testable and implies that low levels and low variability in serum BDNF are associated with poor response to anti-depressive medications, electroconvulsive therapy, and REM sleep deprivation, in patients with depression.
Major depressive disorder (MDD) is associated with stress-induced immune dysregulation and reduced brain-derived neurotrophic factor (BDNF) levels in sensitive brain regions associated with depression.
The association between BDNFVal66Met and SI was modeled using logistic regression adjusted for age and sex, and in secondary analyses also for depression.
Additionally, elevated miR-133b and inhibited CTGF could restrain apoptosis of hippocampal neurons, repress inflammatory reaction, and increase the expression of GFAP, BDNF and neurotransmitters in hippocampal tissues of depression rats, resulting in a protective impact on neural injury in depression rats.
Importantly, early life stressors that affect BDNF production are known to predispose individuals towards the later development of depression or anxiety disorders.
However, little is known about the relationship between memory performance and depression severity, about the course of memory performance during antidepressant treatment as well as about the relationship between memory performance and brain-derived neurotrophic factor (BDNF).
The specific aim of this study was to explore the relationships between biomarkers of neural health: nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), immune health: interleukin 6 (IL-6), c-reactive protein (CRP), and cortisol, as well as the presence of depression, in physically active cannabis users (CU) and non-users (NU).
Reduced levels of brain derived neurotrophic factor (BDNF), through its role in neurogenesis and neuroplasticity, may be involved in the evolution and maintenance of depression.
Therefore, the present study was conducted on the effect of PRLR gene on brain derived neurotrophic factor (BDNF) expression and hippocampal neuron apoptosis through the establishment of CMS-induced depression mouse models, with aims of providing a new and effective therapeutic option for depression.
Magnesium and ketamine have a common mechanism of action in the treatment of depression: an increase in GluN2B (NMDAR subunit) expression is related to the administration of both of the agents, as well as inhibition of phosphorylation of eEF2 (eukaryotic elongation factor 2) in cell culture and increase of the expression of BDNF in the hippocampus.
: We aimed to assess the association between cord blood brain-derived neurotrophic factor (BDNF) concentration and maternal depression during pregnancy.
To evaluate the effect of vortioxetine combined with cognitive behaviour intervention on the level of brain-derived neurotrophic factor (BDNF) in the serum of patients with depression and its therapeutic effect.
Furthermore, acne vulgaris patients with depression showed lower serum BDNF levels (10.96 ± 2.12 ng/ml) compared with acne vulgaris patients without depression (13.85 ± 2.47 ng/ml), as well as with healthy control (14.35 ± 2.70 ng/mg; both P < 0.05).
These results strongly implicate changes in BDNF levels in serum and the nucleus accumbens in the pathophysiology and treatment of early life combined stress-induced depression and highlight the therapeutic potential of escitalopram and new generation antipsychotic blonanserin for treatment-resistant refractory depression.
We investigated the effect of a daily low dose of a phosphodiesterase (PDE) type 5 inhibitor (tadalafil, 5 mg) on depression and levels of brain-derived neurotrophic factor (BDNF) in patients with ED.
Our findings show an association between low serum BDNF and SI in individuals with less than severe and non-active suicidal intent, suggesting that the individual symptom of suicidality may extend the neurotrophic hypothesis of depression to include suicidal ideation within MDD.
This review describes (1) different 5-HT functioning in the embryonic (as neurotrophin) and adult brain (as a neurotransmitter); (2) BDNF as a modulator of 5-HT system and vice versa; (3) the prolonged positive effect of BDNF on genetically and epigenetically defined central nervous system disorders; (4) The 5-HT-BDNF interplay contribution to aggressive behavior, depression, drug addiction, suicide, and stress response; and (5) the role of common second messengers for 5-HT and BDNF signaling in the 5-HT-BDNF interaction.
Moreover, we measured and analysed the brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) levels and the upstream regulation and signal pathways of BDNF and NGF to explore their related mechanisms in this animal model of depression, including calcium-calmodulin dependent protein kinase-II (CaMKII) and cAMP response element-binding (CREB).