Successful Treatment of Depression With Tetrahydrobiopterin

Curtius, Hans−Christoph; Niederwieser, A.; Levine, R.; Lovenberg, Walter; Woggon, B; Angst, J.

doi:10.1016/s0140-6736(83)91837-8

Cited by 90 publications

(27 citation statements)

References 8 publications

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“…Alternatively, targeting the neopterin pathway, in particular, BH4, which is a critical cofactor for monoamine synthesis and is altered in obesity (Finkelstein et al, 1982;Ledochowski et al, 1999;Oxenkrug et al, 2011;Oxenkrug, 2010), may also provide a useful way to reduce adiposity-driven inflammation and related depressive symptoms. This assumption is supported by findings reporting relief of treatment refractory depression by BH4 replacement (Curtius et al, 1983;Pan et al, 2011). Finally, owing to the tight interactions between inflammation and metabolic alterations, including insulin resistance and dyslipidemia, adiposity-driven inflammation may also be targeted by antidiabetic drugs, which have already been shown to display antidepressant properties Pomytkin et al, 2015;Scheen et al, 2015).…”

Section: Pharmacological Strategiesmentioning

confidence: 80%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

141

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Depression and metabolic disorders, including overweight and obesity, appear tightly interrelated. The prevalence of these conditions is concurrently growing worldwide, and both depression and overweight/obesity represent substantial risk factors for multiple medical complications. Moreover, there is now multiple evidence for a bidirectional relationship between depression and increased adiposity, with overweight/obesity being associated with an increased prevalence of depression, and in turn, depression augmenting the risk of weight gain and obesity. Although the reasons for this intricate link between depression and increased adiposity remain unclear, converging clinical and preclinical evidence points to a critical role for inflammatory processes and related alterations of brain functions. In support of this notion, increased adiposity leads to a chronic low-grade activation of inflammatory processes, which have been shown elsewhere to have a potent role in the pathophysiology of depression. It is therefore highly possible that adiposity-driven inflammation contributes to the development of depressive disorders and their growing prevalence worldwide. This review will present recent evidence in support of this hypothesis and will discuss the underlying mechanisms and potential therapeutic targets. Altogether, findings presented here should help to better understand the mechanisms linking adiposity to depression and facilitate the identification of new preventive and/or therapeutic strategies.

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Section: Pharmacological Strategiesmentioning

confidence: 80%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

141

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“…[18][19][20][21] Others have also found a decrease in levels of tetrahydrobiopterin, a natural cofactor for TH, in depressed patients. [22][23][24][25] This evidence seems to indicate that adaptive changes in TH and the onset of action of various antidepressants are linked.…”

Section: Role Of Th In Depressionmentioning

confidence: 94%

Stress, norepinephrine and depression

Leonard

2002

Acta Neuropsychiatr.

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Journal of Psychiatry & Neuroscience S11Stress is an important precipitant factor in depression, and the changes in various body systems that occur in depression are similar to those observed in response to stress. This paper discusses the interactions among the immune, endocrine and norepinephrine systems that are evident in patients with depression, as well as those affected by stress. Many of the stress-induced changes can be reversed by antidepressants, particularly norepinephrine reuptake inhibitors.Le stress est un important facteur catalyseur dans les cas de dépression et les changements subis par les divers systèmes corporels au cours de la dépression ressemblent à ceux qu'on observe face au stress. Cette communication porte sur les interactions entre les systèmes immunitaire, endocrinien et celui de la norépinéphrine, qui sont évidentes chez les patients atteints de dépression, ainsi que chez ceux qui sont touchés par le stress. Il est possible d'inverser un grand nombre de ces changements causés par le stress en utilisant des antidépresseurs et en particulier des inhibiteurs du recaptage de la norépinéphrine.Norepinephrine in depression and mood disorders La norépinéphrine dans la dépression et les troubles psychiques

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“…In a previous genetic investigation of the sepiapterin reductase (SPR) gene, the terminal enzyme in the de novo synthesis of BH 4 (Figure 1), we showed that variation in the SPR promoter influenced individual risk to mood disorders, as well as a having a potential role in response to selective serotonin reuptake inhibitors (SSRIs) in individuals with major depressive disorder (MDD). 4 Curtius et al 5 showed that depressed patients treated with BH 4 showed a marked improvement in mood. Other studies have shown a relationship between BH 4 activity and antidepressants.…”

Section: Introductionmentioning

confidence: 99%

A polymorphism of the GTP-cyclohydrolase I feedback regulator gene alters transcriptional activity and may affect response to SSRI antidepressants

et al. 2010

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Tetrahydrobiopterin (BH 4 ) is an essential cofactor for synthesis of many neurotransmitters including serotonin. In serotonergic neurons, BH 4 is tightly regulated by GTP-cyclohydrolase I feedback regulator (GFRP). Given the pivotal role of the serotonergic system in mood disorders and selective serotonin reuptake inhibitors (SSRIs) antidepressant function, we tested the hypothesis that GFRP gene (GCHFR) variants would modify response to antidepressants in subjects with major depression. Two single nucleotide polymorphisms (rs7164342 and rs7163862) in the GCHFR promoter were identified and occurred as two haplotypes (GA or TT). A multiple regression analysis revealed that homozygous individuals for the TT haplotype were less likely to respond to the SSRI fluoxetine than to the tricyclic antidepressant nortriptyline (P ¼ 0.037). Moreover, the TT haplotype showed a reduced transcription rate in luciferase reporter gene assays, which may impact on BH 4 -mediated neurotransmitter production, thus suggesting a biological process through which GCHFR promoter variants might influence antidepressant response.

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Successful Treatment of Depression With Tetrahydrobiopterin

Cited by 90 publications

References 8 publications

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Stress, norepinephrine and depression

A polymorphism of the GTP-cyclohydrolase I feedback regulator gene alters transcriptional activity and may affect response to SSRI antidepressants

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