Show simple item record

dc.contributor.authorOh, SeungJu Jackie
dc.contributor.authorFan, Xiaoduo
dc.date2022-08-11T08:10:31.000
dc.date.accessioned2022-08-23T17:11:33Z
dc.date.available2022-08-23T17:11:33Z
dc.date.issued2019-06-01
dc.date.submitted2019-08-01
dc.identifier.citation<p>CNS Drugs. 2019 Jun;33(6):539-547. doi: 10.1007/s40263-019-00632-4. <a href="https://doi.org/10.1007/s40263-019-00632-4">Link to article on publisher's site</a></p>
dc.identifier.issn1172-7047 (Linking)
dc.identifier.doi10.1007/s40263-019-00632-4
dc.identifier.pmid30993607
dc.identifier.urihttp://hdl.handle.net/20.500.14038/46305
dc.description.abstractA growing body of literature has elucidated the involvement of the central renin-angiotensin system (RAS) in various neuropsychiatric diseases. While consensus on the exact mechanism of the central RAS in schizophrenia pathophysiology does not currently exist, increasing evidence reveals promise in harnessing the therapeutic potential of RAS modulation in the treatment of schizophrenia. In this review, we examine how the central RAS affects inflammation, glutamate, dopamine, gamma-aminobutyric acid (GABA), and peroxisome proliferator-activated receptor (PPAR)-gamma, all of which are associated with schizophrenia etiology. In addition, a recent study has demonstrated the therapeutic potential of RAS modulators, especially angiotensin II type 1 receptor blockers (ARBs), as adjunctive therapy to the currently available antipsychotic medications for schizophrenia treatment. With a greater understanding of how RAS inhibition directly modulates neurotransmitter balance in the brain, it is possible that compounds with RAS-inhibiting properties could be used to optimize physiological levels of glutamate, dopamine, and GABA, and the balance among the three neurotransmitters, analogously to how antipsychotic medications mediate the dopaminergic pathways. It can be hoped that a novel approach based on this concept, such as adjunctive telmisartan therapy, may offer practical interventional strategies to address currently unmet therapeutic needs in patients with schizophrenia, especially those with treatment-resistant schizophrenia.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=30993607&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1007/s40263-019-00632-4
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectBiochemical Phenomena, Metabolism, and Nutrition
dc.subjectCellular and Molecular Physiology
dc.subjectMental and Social Health
dc.subjectMental Disorders
dc.subjectNervous System
dc.subjectNeuroscience and Neurobiology
dc.subjectPharmacology, Toxicology and Environmental Health
dc.subjectPsychiatry
dc.subjectPsychiatry and Psychology
dc.subjectTherapeutics
dc.titleThe Possible Role of the Angiotensin System in the Pathophysiology of Schizophrenia: Implications for Pharmacotherapy
dc.typeJournal Article
dc.source.journaltitleCNS drugs
dc.source.volume33
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/psych_pp/842
dc.identifier.contextkey15038725
html.description.abstract<p>A growing body of literature has elucidated the involvement of the central renin-angiotensin system (RAS) in various neuropsychiatric diseases. While consensus on the exact mechanism of the central RAS in schizophrenia pathophysiology does not currently exist, increasing evidence reveals promise in harnessing the therapeutic potential of RAS modulation in the treatment of schizophrenia. In this review, we examine how the central RAS affects inflammation, glutamate, dopamine, gamma-aminobutyric acid (GABA), and peroxisome proliferator-activated receptor (PPAR)-gamma, all of which are associated with schizophrenia etiology. In addition, a recent study has demonstrated the therapeutic potential of RAS modulators, especially angiotensin II type 1 receptor blockers (ARBs), as adjunctive therapy to the currently available antipsychotic medications for schizophrenia treatment. With a greater understanding of how RAS inhibition directly modulates neurotransmitter balance in the brain, it is possible that compounds with RAS-inhibiting properties could be used to optimize physiological levels of glutamate, dopamine, and GABA, and the balance among the three neurotransmitters, analogously to how antipsychotic medications mediate the dopaminergic pathways. It can be hoped that a novel approach based on this concept, such as adjunctive telmisartan therapy, may offer practical interventional strategies to address currently unmet therapeutic needs in patients with schizophrenia, especially those with treatment-resistant schizophrenia.</p>
dc.identifier.submissionpathpsych_pp/842
dc.contributor.departmentSchool of Medicine
dc.contributor.departmentPsychotic Disorders Program, UMass Memorial Medical Center
dc.contributor.departmentImplementation Science and Practice Advances Research Center
dc.contributor.departmentDepartment of Psychiatry
dc.source.pages539-547


This item appears in the following Collection(s)

Show simple item record