Serum Concentrations of Nerve Growth Factor and Brain-Derived Neurotrophic Factor in Depressed Patients before and after Antidepressant Treatment

Hellweg, Rainer; Ziegenhorn, Andreas; Heuser, Isabella; Deuschle, Michael

doi:10.1055/s-2007-1004594

Cited by 115 publications

(75 citation statements)

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“…31,32) It is well accepted that impairment of cell proliferation and neurogenesis in the hippocampus of adult mice underlines the pathology of depression and drug or strategy that reverse these defecits exerts commendable effects in depression treatment. 33) ERKs signal pathway is associated with neurotrophic action, cell survival and proliferation.…”

Section: Discussionmentioning

confidence: 99%

Antidepressant Effects of a Plant-Derived Flavonoid Baicalein Involving Extracellular Signal-Regulated Kinases Cascade

Xiong

Jiang

et al. 2011

Biological & Pharmaceutical Bulletin

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Depression is a serious psychiatric disorder that easily causes physical impairment and a high suicide rate.1) Current treatment mainly depends on the traditional therapeutic strategy that affecting serotonin and/or norepinephrine system, but roughly half of affected individuals are inadequately treated by available medications and psychotherapeutic approaches.2,3) Despite tremendous effort, the field has not yet succeeded in developing fundamentally new antidepressants with distinct mechanisms of action. 4)It has been demonstrated that adult neurogenesis in the dentate gyrus (DG) plays a critical role in depression and the therapeutic effects of antidepressants appear to be neurogenesis-dependent. 5) Neurotrophic factors such as brain-derived neurotrophic factor (BDNF), which act as critical regulator of memory and synaptic plasticity, produce the up-regulation of neurogenesis.6) It is well known that BDNF has been shown to enhance neurogenesis. In addition, BDNF initiates TrkB receptor-dependent activation of extracellular signalregulated kinases (ERKs) and exhibits beneficial effect for the treatment of depression. 7) ERKs is the well-studied member of the mitogen-activated protein kinase (MAPK) family and ERK pathway is the major convergence point involved in neurotrophic and other signal pathways that regulates cellular differentiation and neuronal plasticity. [8][9][10] It has been demonstrated that ERK activation can further trigger neurotrophic effects, including neurite growth, neuronal survival and hippocampal neurogenesis.11) Thus, much attention has turned to the role of ERKs in depression. Actually, many classic antidepressant drugs, such as fluoxetine, can reverse the decreased ERK1/2 phosphorylation (p-ERK1/2) induced by depression in the hippocampus.12) By the fact that the therapeutic effects of antidepressants appear to be ERK-related, we postulate that agents that can reverse the decrease in BDNF and p-ERK1/2 caused by depression may produce antidepressant effects.Accumulated evidence has shown that plant-derived flavonoids can produce wide effects including neuroprotection, antioxidant, and regulation of synaptic plasticity and memory enhancement. [13][14][15][16] Recently, it is demonstrated that some flavonoids such as hypericum perforatum and quercetin, display antidepressant effects and attenuate the cognitive deficits caused by major depression. [17][18][19] Baicalein (Bai) is one of the most active flavonoids found in the dry roots of Scutellaria baicalensis Georgi. It is documented that Bai can get across blood-brain barrier (BBB). 13,20) In our previous study, it is shown that Bai protects neurons from free radical-induced damage in vitro and alleviates ischemic brain injury in vivo. 13,21) More importantly, several reports have revealed that Bai stimulates the expression levels of pERK and BDNF in the hippocampus of normal rats. 22) Considering this neurotrophic effect, we postulate that Bai may have an antidepressant-like effect. Thus, the therapeutic role of Bai in animals of depre...

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Section: Discussionmentioning

confidence: 99%

Antidepressant Effects of a Plant-Derived Flavonoid Baicalein Involving Extracellular Signal-Regulated Kinases Cascade

Xiong

Jiang

et al. 2011

Biological & Pharmaceutical Bulletin

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show abstract

“…Indeed, chronic psychological stress, a common component of depression, enhances glucocorticoid release and suppresses NGF mRNA expression in the hippocampus (Alfonso et al, 2004). Furthermore, antidepressant treatments or electroconvulsive shock therapy increases the expression and concentrations of NGF in the brain (Alfonso et al, 2006;Hellweg et al, 2008). However, dexamethasone or corticosterone treatment has been also reported to increase NGF expression in the several brain regions, including the hippocampus (Shi et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Increased Phospholipase A2 Activity and Inflammatory Response But Decreased Nerve Growth Factor Expression in the Olfactory Bulbectomized Rat Model of Depression: Effects of Chronic Ethyl-Eicosapentaenoate Treatment

Song¹,

Zhang²,

Manku³

2009

J. Neurosci.

167

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An increased inflammatory response and deficient synthesis of neurotrophic factors (NTFs) may contribute to the etiology of depression. However, the interrelationship between inflammation and NTFs is unknown. Recently, ethyl-eicosapentaenoate (EPA) has been used to treat depression. The mechanism by which EPA benefits depression is also unclear. Using the olfactory bulbectomized (OB) rat model of depression, this study evaluated two pathways from bulbectomy to the induction of depression-like changes (the inflammation-hypothalamic-pituitary-adrenal axis-stress response pathway and inflammation-nerve growth factor-memory pathway) and the effect of EPA on these pathways. When compared with sham-operated rats fed a control diet, significantly increased locomotor and rearing activities in an "open field," impaired memory in the Morris water maze, increased expression of corticotrophin-releasing factor (CRF), and increased secretion of corticosterone were found in OB rats. mRNA expression of nerve growth factor (NGF) was significantly lower in the hippocampus, and phospholipase A2 (PLA2) was higher in the hypothalamus; this change was associated with increased interleukin-1␤ (IL-1␤) and prostaglandin E2 (PGE2) in the serum and brain. EPA treatments normalized these behavioral impairments and reduced CRF expression and corticosterone secretion. EPA also reduced serum concentrations of IL-1␤ and PGE2, but reversed NGF reduction. Similar to the effects of EPA, the anti-inflammatory drug celecoxib significantly reduced blood PGE2, IL-1␤, and corticosterone concentrations and increased NGF expression in OB rats. Furthermore, anti-NGF treatment blocked EPA effects on behavior. These results suggest that an interaction exists between inflammation and NGF in the depression model. EPA may improve depression via its anti-inflammation properties and the upregulation of NGF.

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“…The emission was measured with a fl uorescence photometer (excitation wavelength 485 nm, emission wavelength 538 nm). This assay has a detection limit of 0.7 pg/mL serum BDNF, the coeffi cients of inter-and intra-assay variation are 34.1 % and 6.7 %, respectively [ 23 ] . Since the intra-assay variation is much less than the inter-assay variation, the corresponding pre-and post-treatment samples of patients were always measured in the same BDNF assay.…”

Section: Laboratory Methodsmentioning

confidence: 99%

Changes of Serum Concentrations of Brain-Derived Neurotrophic Factor (BDNF) during Treatment with Venlafaxine and Mirtazapine: Role of Medication and Response to Treatment

et al. 2012

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Introduction: Depression, stress and antidepressant treatment have been found to modulate the expression of brain-derived neurotrophic factor (BDNF). Recent research suggests that serum BDNF concentration is reduced in depression and that antidepressant treatment leads to an increase in serum BDNF concentration. Methods: We studied depressed patients receiving a randomized antidepressant treatment with either mirtazapine (n=29) or venlafaxine (n=27) for 28 days in a prospective design. Changes in the concentrations of serum neurotrophins in response to antidepressant treatment were assessed. Results: There was a significant ?treatment? by ?medication? interaction effect on BDNF serum concentrations that indicated a decline of BDNF in venlafaxine-treated patients (7.82?3.75?7.18?5.64?ng/mL), while there was an increase in mirtazapine-treated patients (7.64?6.23?8.50?5.37?ng/mL). There was a trend for a ?treatment? by ?remission? interaction with a favourable clinical course being related to increasing serum BDNF. Discussion: Changes in BDNF serum concentrations as a result of antidepressant therapy depend on the antidepressant and potentially on the clinical course.

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Serum Concentrations of Nerve Growth Factor and Brain-Derived Neurotrophic Factor in Depressed Patients before and after Antidepressant Treatment

Abstract: Changes in BDNF serum concentrations as a result of antidepressant therapy depend on the antidepressant instead of being a general characteristic of response to antidepressant treatment.

Cited by 115 publications

References 54 publications

Antidepressant Effects of a Plant-Derived Flavonoid Baicalein Involving Extracellular Signal-Regulated Kinases Cascade

Antidepressant Effects of a Plant-Derived Flavonoid Baicalein Involving Extracellular Signal-Regulated Kinases Cascade

Increased Phospholipase A2 Activity and Inflammatory Response But Decreased Nerve Growth Factor Expression in the Olfactory Bulbectomized Rat Model of Depression: Effects of Chronic Ethyl-Eicosapentaenoate Treatment

Changes of Serum Concentrations of Brain-Derived Neurotrophic Factor (BDNF) during Treatment with Venlafaxine and Mirtazapine: Role of Medication and Response to Treatment

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