dc.creatorMaes, Michael
dc.creatorNowak, Gabriel
dc.creatorCaso, Javier R.
dc.creatorCarlos Leza, Juan
dc.creatorSong, Cai
dc.creatorKubera, Marta
dc.creatorKlein, Hans
dc.creatorGalecki, Piotr
dc.creatorNoto, Cristiano [UNIFESP]
dc.creatorGlaab, Enrico
dc.creatorBalling, Rudi
dc.creatorBerk, Michael
dc.date.accessioned2020-08-14T13:44:29Z
dc.date.accessioned2022-10-07T20:30:37Z
dc.date.available2020-08-14T13:44:29Z
dc.date.available2022-10-07T20:30:37Z
dc.date.created2020-08-14T13:44:29Z
dc.date.issued2016
dc.identifierMolecular Neurobiology. New York, v. 53, n. 5, p. 2927-2935, 2016.
dc.identifier0893-7648
dc.identifierhttps://repositorio.unifesp.br/handle/11600/57694
dc.identifier10.1007/s12035-015-9183-5
dc.identifierWOS:000377935400019
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/4018889
dc.description.abstractMeta-analyses confirm that depression is accompanied by signs of inflammation including increased levels of acute phase proteins, e.g., C-reactive protein, and pro-inflammatory cytokines, e.g., interleukin-6. Supporting the translational significance of this, a meta-analysis showed that anti-inflammatory drugs may have antidepressant effects. Here, we argue that inflammation and depression research needs to get onto a new track. Firstly, the choice of inflammatory biomarkers in depression research was often too selective and did not consider the broader pathways. Secondly, although mild inflammatory responses are present in depression, other immune-related pathways cannot be disregarded as new drug targets, e.g., activation of cell-mediated immunity, oxidative and nitrosative stress (O&NS) pathways, autoimmune responses, bacterial translocation, and activation of the toll-like receptor and neuroprogressive pathways. Thirdly, anti-inflammatory treatments are sometimes used without full understanding of their effects on the broader pathways underpinning depression. Since many of the activated immune-inflammatory pathways in depression actually confer protection against an overzealous inflammatory response, targeting these pathways may result in unpredictable and unwanted results. Furthermore, this paper discusses the required improvements in research strategy, i.e., path and drug discovery processes, omics-based techniques, and systems biomedicine methodologies. Firstly, novel methods should be employed to examine the intracellular networks that control and modulate the immune, O&NS and neuroprogressive pathways using omics-based assays, including genomics, transcriptomics, proteomics, metabolomics, epigenomics, immunoproteomics and metagenomics. Secondly, systems biomedicine analyses are essential to unravel the complex interactions between these cellular networks, pathways, and the multifactorial trigger factors and to delineate new drug targets in the cellular networks or pathways. Drug discovery processes should delineate new drugs targeting the intracellular networks and immune-related pathways.
dc.languageeng
dc.publisherSpringer
dc.relationMolecular Neurobiology
dc.rightsAcesso restrito
dc.subjectDepression
dc.subjectImmune
dc.subjectInflammation
dc.subjectNeuroprogression
dc.subjectOxidative and nitrosative stress
dc.subjectLeaky gut
dc.subjectIDO
dc.subjectTRYCATs
dc.titleToward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research
dc.typeArtigo


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