Neuroinflammation and glial cell activation in mental disorders
Autor(a) principal: | |
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Data de Publicação: | 2020 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | https://repositorio.unifesp.br/xmlui/handle/11600/62144 |
Resumo: | Mental disorders (MDs) are highly prevalent and potentially debilitating complex disorders which causes remain elusive. Looking into deeper aspects of etiology or pathophysiology underlying these diseases would be highly beneficial, as the scarce knowledge in mechanistic and molecular pathways certainly represents an important limitation. Association between MDs and inflammation/neuroinflammation has been widely discussed and accepted by many, as high levels of pro-inflammatory cytokines were reported in patients with several MDs, such as schizophrenia (SCZ), bipolar disorder (BD) and major depression disorder (MDD), among others. Correlation of pro-inflammatory markers with symptoms intensity was also reported. However, the mechanisms underlying the inflammatory dysfunctions observed in MDs are not fully understood yet. In this context, microglial dysfunction has recently emerged as a possible pivotal player, as during the neuroinflammatory response, microglia can be over-activated, and excessive production of pro-inflammatory cytokines, which can modify the kynurenine and glutamate signaling, is reported. Moreover, microglial activation also results in increased astrocyte activity and consequent glutamate release, which are both toxic to the Central Nervous System (CNS). Also, as a result of increased microglial activation in MDs, products of the kynurenine pathway were shown to be changed, influencing then the dopaminergic, serotonergic, and glutamatergic signaling pathways. Therefore, in the present review, we aim to discuss how neuroinflammation impacts on glutamate and kynurenine signaling pathways, and how they can consequently influence the monoaminergic signaling. The consequent association with MDs main symptoms is also discussed. As such, this work aims to contribute to the field by providing insights into these alternative pathways and by shedding light on potential targets that could improve the strategies for pharmacological intervention and/or treatment protocols to combat the main pharmacologically unmatched symptoms of MDs, as the SCZ. |
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Repositório Institucional da UNIFESP |
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Almeida, Priscila G. C.Nani, João VictorOses, Jean PierreBrietzke, Elisa [UNIFESP]Hayashi, Mirian A F [UNIFESP]http://lattes.cnpq.br/5559309395232147http://lattes.cnpq.br/2938015553073591http://lattes.cnpq.br/9741366667739336http://lattes.cnpq.br/1198445675076270http://lattes.cnpq.br/54725122449935462021-10-29T09:12:04Z2021-10-29T09:12:04Z2020-02https://repositorio.unifesp.br/xmlui/handle/11600/62144Mental disorders (MDs) are highly prevalent and potentially debilitating complex disorders which causes remain elusive. Looking into deeper aspects of etiology or pathophysiology underlying these diseases would be highly beneficial, as the scarce knowledge in mechanistic and molecular pathways certainly represents an important limitation. Association between MDs and inflammation/neuroinflammation has been widely discussed and accepted by many, as high levels of pro-inflammatory cytokines were reported in patients with several MDs, such as schizophrenia (SCZ), bipolar disorder (BD) and major depression disorder (MDD), among others. Correlation of pro-inflammatory markers with symptoms intensity was also reported. However, the mechanisms underlying the inflammatory dysfunctions observed in MDs are not fully understood yet. In this context, microglial dysfunction has recently emerged as a possible pivotal player, as during the neuroinflammatory response, microglia can be over-activated, and excessive production of pro-inflammatory cytokines, which can modify the kynurenine and glutamate signaling, is reported. Moreover, microglial activation also results in increased astrocyte activity and consequent glutamate release, which are both toxic to the Central Nervous System (CNS). Also, as a result of increased microglial activation in MDs, products of the kynurenine pathway were shown to be changed, influencing then the dopaminergic, serotonergic, and glutamatergic signaling pathways. Therefore, in the present review, we aim to discuss how neuroinflammation impacts on glutamate and kynurenine signaling pathways, and how they can consequently influence the monoaminergic signaling. The consequent association with MDs main symptoms is also discussed. As such, this work aims to contribute to the field by providing insights into these alternative pathways and by shedding light on potential targets that could improve the strategies for pharmacological intervention and/or treatment protocols to combat the main pharmacologically unmatched symptoms of MDs, as the SCZ.ElsevierBrain, Behavior, & Immunity - HealthInflammationMental disordersGliaMicroglial activationSchizophreniaNeuroinflammation and glial cell activation in mental disordersinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessengreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPEscola Paulista de Medicina (EPM)FarmacologiaFarmacologiaORIGINAL1-s2.0-S2666354619300353-main.pdf1-s2.0-S2666354619300353-main.pdfapplication/pdf799728${dspace.ui.url}/bitstream/11600/62144/1/1-s2.0-S2666354619300353-main.pdf0d420ad2364594d2dc546814769afa78MD51open 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dc.title.pt_BR.fl_str_mv |
Neuroinflammation and glial cell activation in mental disorders |
title |
Neuroinflammation and glial cell activation in mental disorders |
spellingShingle |
Neuroinflammation and glial cell activation in mental disorders Almeida, Priscila G. C. Inflammation Mental disorders Glia Microglial activation Schizophrenia |
title_short |
Neuroinflammation and glial cell activation in mental disorders |
title_full |
Neuroinflammation and glial cell activation in mental disorders |
title_fullStr |
Neuroinflammation and glial cell activation in mental disorders |
title_full_unstemmed |
Neuroinflammation and glial cell activation in mental disorders |
title_sort |
Neuroinflammation and glial cell activation in mental disorders |
author |
Almeida, Priscila G. C. |
author_facet |
Almeida, Priscila G. C. Nani, João Victor Oses, Jean Pierre Brietzke, Elisa [UNIFESP] Hayashi, Mirian A F [UNIFESP] |
author_role |
author |
author2 |
Nani, João Victor Oses, Jean Pierre Brietzke, Elisa [UNIFESP] Hayashi, Mirian A F [UNIFESP] |
author2_role |
author author author author |
dc.contributor.authorLattes.pt_BR.fl_str_mv |
http://lattes.cnpq.br/5559309395232147 http://lattes.cnpq.br/2938015553073591 http://lattes.cnpq.br/9741366667739336 |
dc.contributor.authorLattes.none.fl_str_mv |
http://lattes.cnpq.br/1198445675076270 http://lattes.cnpq.br/5472512244993546 |
dc.contributor.author.fl_str_mv |
Almeida, Priscila G. C. Nani, João Victor Oses, Jean Pierre Brietzke, Elisa [UNIFESP] Hayashi, Mirian A F [UNIFESP] |
dc.subject.por.fl_str_mv |
Inflammation Mental disorders Glia Microglial activation Schizophrenia |
topic |
Inflammation Mental disorders Glia Microglial activation Schizophrenia |
description |
Mental disorders (MDs) are highly prevalent and potentially debilitating complex disorders which causes remain elusive. Looking into deeper aspects of etiology or pathophysiology underlying these diseases would be highly beneficial, as the scarce knowledge in mechanistic and molecular pathways certainly represents an important limitation. Association between MDs and inflammation/neuroinflammation has been widely discussed and accepted by many, as high levels of pro-inflammatory cytokines were reported in patients with several MDs, such as schizophrenia (SCZ), bipolar disorder (BD) and major depression disorder (MDD), among others. Correlation of pro-inflammatory markers with symptoms intensity was also reported. However, the mechanisms underlying the inflammatory dysfunctions observed in MDs are not fully understood yet. In this context, microglial dysfunction has recently emerged as a possible pivotal player, as during the neuroinflammatory response, microglia can be over-activated, and excessive production of pro-inflammatory cytokines, which can modify the kynurenine and glutamate signaling, is reported. Moreover, microglial activation also results in increased astrocyte activity and consequent glutamate release, which are both toxic to the Central Nervous System (CNS). Also, as a result of increased microglial activation in MDs, products of the kynurenine pathway were shown to be changed, influencing then the dopaminergic, serotonergic, and glutamatergic signaling pathways. Therefore, in the present review, we aim to discuss how neuroinflammation impacts on glutamate and kynurenine signaling pathways, and how they can consequently influence the monoaminergic signaling. The consequent association with MDs main symptoms is also discussed. As such, this work aims to contribute to the field by providing insights into these alternative pathways and by shedding light on potential targets that could improve the strategies for pharmacological intervention and/or treatment protocols to combat the main pharmacologically unmatched symptoms of MDs, as the SCZ. |
publishDate |
2020 |
dc.date.issued.fl_str_mv |
2020-02 |
dc.date.accessioned.fl_str_mv |
2021-10-29T09:12:04Z |
dc.date.available.fl_str_mv |
2021-10-29T09:12:04Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://repositorio.unifesp.br/xmlui/handle/11600/62144 |
url |
https://repositorio.unifesp.br/xmlui/handle/11600/62144 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.pt_BR.fl_str_mv |
Brain, Behavior, & Immunity - Health |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.publisher.none.fl_str_mv |
Elsevier |
publisher.none.fl_str_mv |
Elsevier |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
bitstream.url.fl_str_mv |
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repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1802764151690362880 |