Decreased plasma BDNF level in depressive patients

Lee, Bun-Hee; Kim, Han Sung; Park, Se-Hyuck; Kim, Yong Ku

doi:10.1016/j.jad.2006.11.005

Cited by 281 publications

(190 citation statements)

References 20 publications

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“…8 studies comparing serum BDNF levels in depressed subjects before and after antidepressant treatment were identified and included for our second analysis. Although there are now a few recent studies suggesting plasma BDNF content is also decreased in depressed subjects (19,(21)(22)(23), this data was not included in this analysis in order to minimize potential confounds.…”

Section: Studiesmentioning

confidence: 99%

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

Sen

Duman

Sanacora

2008

Biological Psychiatry

1,091

715

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Section: Studiesmentioning

confidence: 99%

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

Sen

Duman

Sanacora

2008

Biological Psychiatry

1,091

715

View full text Add to dashboard Cite

show abstract

“…A clinical study in 2004 has shown that serum BDNF levels negatively correlated with the depression-related personality traits (Lang et al, 2004). Afterwards, serum and plasma BDNF levels have been found decreased in patients with major depressive disorder (MDD) (Lee et al, 2007;Piccinni et al, 2008). These clinical studies have suggested that peripheral BDNF levels can serve as a biomarker for depression.…”

Section: Introductionmentioning

confidence: 99%

ProBDNF Signaling Regulates Depression-Like Behaviors in Rodents under Chronic Stress

Bai

Ruan

Yang

et al. 2016

Neuropsychopharmacol

104

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Chronic exposure to stressful environment is a key risk factor contributing to the development of depression. However, the mechanisms involved in this process are still unclear. Brain-derived neurotropic factor (BDNF) has long been investigated for its positive role in regulation of mood, although the role of its precursor, proBDNF, in regulation of mood is not known. In this study, using an unpredictable chronic mild stress (UCMS) paradigm we found that the protein levels of proBDNF were increased in the neocortex and hippocampus of stressed mice and this UCMS-induced upregulation of proBDNF was abolished by chronic administration of fluoxetine. We then established a rat model of UCMS and found that the expression of proBDNF/p75 NTR /sortilin was upregulated, whereas the expression of mature BDNF and TrkB was downregulated in both neocortex and hippocampus of chronically stressed rats. Finally, we found that the injection of anti-proBDNF antibody via intracerebroventricular (i.c.v.) and intraperitoneal (i.p.) approaches into the UCMS rats significantly reversed the stress-induced depression-like behavior and restored the exploratory activity and spine growth. Although intramuscular injection of AAV-proBDNF did not exacerbate the UCMS-elicited rat mood-related behavioral or pathological abnormalities, i.c.v. injection of AAV-proBDNF increased the depression-like behavior in naive rats. Our findings suggest that proBDNF plays a role in the development of chronic stress-induced mood disturbances in rodents. Central (i.c.v.) or peripheral (i.p.) inhibition of proBDNF by injecting specific antiproBDNF antibodies may provide a novel therapeutic approach for the treatment of stress-related mood disorders.

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“…Decreases in BDNF gene expression are closely correlated with neurodegenerative diseases (Canals et al 2004) and mood disorders (Weickert et al 2003;Lee et al 2007). Owing to the opposing roles of NMDA receptors in neuronal survival and death, therapeutic strategies that use NMDA receptor antagonists to attenuate excitotoxic neuronal death have encountered the challenge of preserving the NMDA receptormediated neurotrophism (Waxman and Lynch 2005;Lipton 2004).…”

mentioning

confidence: 99%

Knockdown of the aryl hydrocarbon receptor attenuates excitotoxicity and enhances NMDA‐induced BDNF expression in cortical neurons

Lin

Chen

Chou

et al. 2009

Journal of Neurochemistry

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NMDA receptors play dual and opposing roles in neuronal survival by mediating the activity‐dependent neurotrophic signaling and excitotoxic cell death via synaptic and extrasynaptic receptors, respectively. In this study, we demonstrate that the aryl hydrocarbon receptor (AhR), also known as the dioxin receptor, is involved in the expression and the opposing activities of NMDA receptors. In primary cultured cortical neurons, we found that NMDA excitotoxicity is significantly enhanced by an AhR agonist 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin, and AhR knockdown with small interfering RNA significantly reduces NMDA excitotoxicity. AhR knockdown also significantly reduces NMDA‐increases intracellular calcium concentration, NMDA receptor expression and surface presentation, and moderately decreases the NMDA receptor‐mediated spontaneous as well as miniature excitatory post‐synaptic currents. However, AhR knockdown significantly enhances the bath NMDA application– but not synaptic NMDA receptor‐induced brain‐derived neurotrophic factor (BDNF) gene expression, and activating AhR reduces the bath NMDA‐induced BDNF expression. Furthermore, AhR knockdown reveals the calcium dependency of NMDA‐induced BDNF expression and the binding activity of cAMP‐responsive element binding protein (CREB) and its calcium‐dependent coactivator CREB binding protein (CBP) to the BDNF promoter upon NMDA treatment. Together, our results suggest that AhR opposingly regulates NMDA receptor‐mediated excitotoxicity and neurotrophism possibly by differentially regulating the expression of synaptic and extrasynaptic NMDA receptors.

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Decreased plasma BDNF level in depressive patients

Cited by 281 publications

References 20 publications

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

ProBDNF Signaling Regulates Depression-Like Behaviors in Rodents under Chronic Stress

Knockdown of the aryl hydrocarbon receptor attenuates excitotoxicity and enhances NMDA‐induced BDNF expression in cortical neurons

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