Inflammation, serotonin and major depression.
Curr Drug Targets
; 14(5): 571-7, 2013 May 01.
Article
em En
| MEDLINE
| ID: mdl-23531160
ABSTRACT
The understanding of the neurobiological processes leading to major depressive disorder (MDD) is an active field of research in the scientific community. For years, the alteration of monoamine neurotransmission, in particular serotonin (5-HT), has been considered the most significant pathophysiological mechanism of the disorder. However, biological data supporting the postulated MDD-related monoamine alterations have been inconclusive, and the use of monoaminergic antidepressants has not yielded the expected results. In the last few years, it has been demonstrated that inflammatory pathways have a significant role in the pathophysiology of MDD. According to the cytokine hypothesis, the disorder would be due to a stress-related increased production of cytokines, including interleukins, tumor necrosis factor- α and interferon- α and γ . These, in turns, would cause the activation of the indoleamine 2,3 dioxygenase (IDO), with subsequent production of tryptophan (TRP) catabolites along the IDO pathway (TRYCATs) and decreased availability of TRP and 5-HT. Besides monoamines, other molecular mechanisms, as those within the inflammatory pathways, should be taken into account in the attempt to clarify the pathophysiology of MDD and to improve its treatment.
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Bases de dados:
MEDLINE
Assunto principal:
Serotonina
/
Transtorno Depressivo Maior
/
Inflamação
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Curr Drug Targets
Assunto da revista:
TERAPIA POR MEDICAMENTOS
Ano de publicação:
2013
Tipo de documento:
Article
País de afiliação:
Itália