{"title":"炎症对谷氨酸的影响是情绪障碍神经进展的一个途径。","authors":"Ebrahim Haroon, Andrew H Miller","doi":"10.1159/000470805","DOIUrl":null,"url":null,"abstract":"<p><p>Neuroprogression is a term used to describe worsening psychopathology, poor treatment response, and declining cognitive and functional outcomes among patients with chronic mental disorders. Chronic inflammatory activation and glutamate-mediated excitotoxicity are two key etiological factors implicated in the development of neuroprogression. In this chapter, we hypothesize that the association between chronic inflammatory activation, neuroprogression, and glutamate dysregulation might be mediated by glial dysfunction. The role played by other mechanisms that increase glutamatergic activity, including oxidative stress and kynurenine pathway activation, will also be discussed, albeit briefly. We will conclude by providing a mechanistic model that draws upon our previous research, to link neuroimmune/neurotransmitter dysregulation to disrupted local neural activity and brain network connectivity eventually leading to a neuroprogressive course and associated clinical outcomes.</p>","PeriodicalId":74212,"journal":{"name":"Modern trends in pharmacopsychiatry","volume":"31 ","pages":"37-55"},"PeriodicalIF":0.0000,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000470805","citationCount":"18","resultStr":"{\"title\":\"Inflammation Effects on Glutamate as a Pathway to Neuroprogression in Mood Disorders.\",\"authors\":\"Ebrahim Haroon, Andrew H Miller\",\"doi\":\"10.1159/000470805\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Neuroprogression is a term used to describe worsening psychopathology, poor treatment response, and declining cognitive and functional outcomes among patients with chronic mental disorders. Chronic inflammatory activation and glutamate-mediated excitotoxicity are two key etiological factors implicated in the development of neuroprogression. In this chapter, we hypothesize that the association between chronic inflammatory activation, neuroprogression, and glutamate dysregulation might be mediated by glial dysfunction. The role played by other mechanisms that increase glutamatergic activity, including oxidative stress and kynurenine pathway activation, will also be discussed, albeit briefly. We will conclude by providing a mechanistic model that draws upon our previous research, to link neuroimmune/neurotransmitter dysregulation to disrupted local neural activity and brain network connectivity eventually leading to a neuroprogressive course and associated clinical outcomes.</p>\",\"PeriodicalId\":74212,\"journal\":{\"name\":\"Modern trends in pharmacopsychiatry\",\"volume\":\"31 \",\"pages\":\"37-55\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1159/000470805\",\"citationCount\":\"18\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Modern trends in pharmacopsychiatry\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000470805\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Modern trends in pharmacopsychiatry","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000470805","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Inflammation Effects on Glutamate as a Pathway to Neuroprogression in Mood Disorders.
Neuroprogression is a term used to describe worsening psychopathology, poor treatment response, and declining cognitive and functional outcomes among patients with chronic mental disorders. Chronic inflammatory activation and glutamate-mediated excitotoxicity are two key etiological factors implicated in the development of neuroprogression. In this chapter, we hypothesize that the association between chronic inflammatory activation, neuroprogression, and glutamate dysregulation might be mediated by glial dysfunction. The role played by other mechanisms that increase glutamatergic activity, including oxidative stress and kynurenine pathway activation, will also be discussed, albeit briefly. We will conclude by providing a mechanistic model that draws upon our previous research, to link neuroimmune/neurotransmitter dysregulation to disrupted local neural activity and brain network connectivity eventually leading to a neuroprogressive course and associated clinical outcomes.