Angiogenic factors in patients with current major depressive disorder comorbid with borderline personality disorder

Kahl, Kai G.; Bens, Susanne; Ziegler, Kristin; Rudolf, Sebastian; Kordon, Andreas; Dibbelt, L.; Schweiger, Ulrich

doi:10.1016/j.psyneuen.2008.09.016

Cited by 103 publications

(94 citation statements)

References 33 publications

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“…Chronic stress exposure has been shown to decrease and antidepressant administration to increase hippocampal VEGF [71,70]. Consistent with these results, it has been reported that VEGF expression and blood levels are increased in patients with depression and that antidepressant treatment reverses these effects [72,73]. …”

Section: Depression As a Cardiovascular Diseasementioning

confidence: 63%

“…Neurotrophin-3 (NT-3) and nerve growth factor (NGF) also influence adult hippocampal neurogenesis and plasticity and thereby could contribute to stress-induced cellular and behavioral deficits, and antidepressant responses [151,152,153,154,155]. Other growth factors which have been shown to be changed in depression include glial cell line-derived neurotrophic factor (GDNF) and fibroblast growth factor-2 (FGF-2) [73,156]. At least FGF-2 can be upregulated by antidepressant treatment [157].…”

Section: Depression As a Neurodegenerative Disordermentioning

confidence: 99%

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Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Lang

Borgwardt²

2013

Cell Physiol Biochem

6,202

229

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Depression is a multicausal disorder and has been associated with the risk to develop cancer, dementia, diabetes, epilepsy and stroke. As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. As a cardiovascular disease a close relationship exists between depression and blood pressure, heart rate, norepinephrine, sympathetic tone, vascular resistance, blood viscosity, plasma volume, intima thickness and atherosclerosis. Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. As an endocrinological and stress disorder depression has been connected with the concentration of free T₄, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. Nutritional factors might influence depression risk, i.e. the consumption of folate, omega-3 fatty acids, monounsaturated fatty acids, olive oil, fish, fruits, vegetables, nuts, legumes, vitamin B6 and vitamin B12. The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. In this context, a fast neuroprotective and antidepressant effect has also been observed by ketamine, which acts via the glutamatergic system. Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. Alternative, causative or also easy available treatment strategies beyond serotonin and noradrenaline reuptake inhibition might be a major topic of future psychiatric care. In this review, an attempt is made to overview concepts of the disease and search for perspectives on antidepressant treatment strategies beyond approved medications.

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Section: Depression As a Cardiovascular Diseasementioning

confidence: 63%

Section: Depression As a Neurodegenerative Disordermentioning

confidence: 99%

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Lang

Borgwardt²

2013

Cell Physiol Biochem

6,202

229

View full text Add to dashboard Cite

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“…However, there are considerable discrepancies among studies investigating VEGF in depression. While some studies have reported increased VEGF mRNA (Berent et al, 2014;Iga et al, 2007), serum (Berent et al, 2014;Kahl et al, 2009) or plasma (Lee and Kim, 2012;Takebayashi et al, 2010) levels in patients with MDD, others have found significant decreases in VEGF peripheral levels in depression (Dome et al, 2009;Isung et al, 2012;Katsuura et al, 2011) or no difference between patients with MDD and healthy controls (Kotan et al, 2012;Ventriglia et al, 2009). A recent review assessing clinical studies on VEGF and depression speculated that elevation in VEGF levels in patients with MDD appears to be due to the response to the perceived stress associated with depression resulting in an attempted neuroprotective effect, whereas decreased levels of VEGF seem to be observed in treatment-resistant depressed patients whose brains are less able to undergo neurogenesis processes (Clark-Raymond and Halaris, 2013).…”

Section: Discussionmentioning

confidence: 99%

Insufficient glucocorticoid signaling and elevated inflammation in coronary heart disease patients with comorbid depression

Nikkheslat

Zunszain

Horowitz

et al. 2015

Brain, Behavior, and Immunity

126

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Coronary heart disease (CHD) and depression are very common and often co-existing disorders. In addition to psychological and social morbidity, depression exacerbates adverse cardiac outcomes in CHD patients. Inflammation has been proposed as one of the mechanisms involved in the association between these two debilitating diseases. Therefore, the present study aimed to evaluate inflammatory responses as well as to investigate the pathophysiological mechanisms underlying the putative inflammatory activation in CHD patients with and without depression, by assessing the function of two important biological factors regulating inflammation, the hypothalamus-pituitary-adrenal (HPA) axis and the glucocorticoid receptor (GR). Eighty-three CHD patients with (n=28) and without (n=55) comorbid depression were recruited from primary care services in South London. Depression status was assessed by means of Clinical Interview Schedule Revised for diagnosis of depression, and Beck Depression Inventory for the presence of depressive symptoms. Serum C-reactive protein (CRP), plasma vascular endothelial growth factor (VEGF), and plasma and salivary cortisol were measured using commercially available ELISA kits. Gene expression of GR and interleukin-6 (IL-6) were conducted via qPCR. GR sensitivity was evaluated in vitro in isolated peripheral blood mononuclear cells using the dexamethasone inhibition of lipopolysaccharide-stimulated IL-6 levels. Serum levels of kynurenine pathway metabolites were measured using high performance liquid chromatography. Our results show that CHD patients with depression had higher levels of CRP, IL-6 gene expression, and VEGF compared with CHD non-depressed, as well as lower plasma and saliva cortisol levels. The CHD depressed group also exhibited a reduction in GR expression and sensitivity. Finally, tryptophan levels were significantly lower in patients with depression, who also showed an increased kynurenine/tryptophan ratio. In conclusion, CHD patients with depression had elevated levels of inflammation in the context of HPA axis hypoactivity, GR resistance, and increased activation of the kynurenine pathway. Reduced cortisol bioavailability and attenuated glucocorticoid responsiveness due to decreased expression and sensitivity of GR may lead to insufficient glucocorticoid signaling and thus elevation of inflammation in these patients.

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“…Kahl and colleagues found increased concentrations of VEGF in nonmedicated depressive patients with borderline personality disorder in comparison with healthy controls [Kahl et al 2009]. Iga and colleagues had previously suggested that a higher expression of VEGF mRNA in the peripheral leucocytes might be associated with the depressive state [Iga et al 2007].…”

Section: Discussionmentioning

confidence: 99%

Serum brain-derived neurotrophic factor, vascular endothelial growth factor and leptin levels in patients with a diagnosis of severe major depressive disorder with melancholic features

Kotan¹,

Sarandöl²,

Kırhan³

et al. 2012

Therapeutic Advances in Psychopharmacology

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Abstract:Objective: Brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF) and leptin have been hypothesized to be involved in the neurobiology of depression. The aim of this study was to investigate BDNF, VEGF and leptin levels in patients with severe melancholic depression. Methods: A total of 40 drug-free patients with major depressive disorder (MDD) with melancholic features and 40 healthy controls were included in the study. Demographic information, psychiatric evaluation and physical examination were documented for both groups. Serum BDNF, VEGF levels were determined by enzyme-linked immunosorbent assay and leptin with radioimmunoassay methods. The Hamilton Depression Rating Scale and Hamilton Anxiety Rating Scale were applied to the patients. Results: There were no significant differences in serum BDNF, VEGF and leptin levels between the patient and control groups. There was a negative correlation between BDNF levels and the number of depressive episodes. It was noted that VEGF levels decreased with increasing severity of depression. Conclusions: These findings suggest that BDNF levels might be associated with the recurrence of depression and VEGF levels might be a determinant of the severity of depression.

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Angiogenic factors in patients with current major depressive disorder comorbid with borderline personality disorder

Cited by 103 publications

References 33 publications

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Insufficient glucocorticoid signaling and elevated inflammation in coronary heart disease patients with comorbid depression

Serum brain-derived neurotrophic factor, vascular endothelial growth factor and leptin levels in patients with a diagnosis of severe major depressive disorder with melancholic features

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