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Neural Basis of Anhedonia and Amotivation in Patients with Schizophrenia: The Role of Reward System

DC Field Value Language
dc.contributor.author김재진-
dc.date.accessioned2018-11-27T16:56:04Z-
dc.date.available2018-11-27T16:56:04Z-
dc.date.issued2015-
dc.identifier.issn1570-159X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/165900-
dc.description.abstractAnhedonia, the inability to feel pleasure, and amotivation, the lack of motivation, are two prominent negative symptoms of schizophrenia, which contribute to the poor social and occupational behaviors in the patients. Recently growing evidence shows that anhedonia and amotivation are tied together, but have distinct neural correlates. It is important to note that both of these symptoms may derive from deficient functioning of the reward network. A further analysis into the neuroimaging findings of schizophrenia shows that the neural correlates overlap in the reward network including the ventral striatum, anterior cingulate cortex and orbitofrontal cortex. Other neuroimaging studies have demonstrated the involvement of the default mode network in anhedonia. The identification of aspecific deficit in hedonic and motivational capacity may help to elucidate the mechanisms behind social functioning deficits in schizophrenia, and may also lead to more targeted treatment of negative symptoms-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherBentham Science Publishers-
dc.relation.isPartOfCURRENT NEUROPHARMACOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnhedonia/physiology*-
dc.subject.MESHAnimals-
dc.subject.MESHBrain/physiopathology*-
dc.subject.MESHHumans-
dc.subject.MESHMotivation/physiology*-
dc.subject.MESHReward-
dc.subject.MESHSchizophrenia/diagnosis-
dc.subject.MESHSchizophrenia/physiopathology*-
dc.subject.MESHSchizophrenic Psychology*-
dc.titleNeural Basis of Anhedonia and Amotivation in Patients with Schizophrenia: The Role of Reward System-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Psychiatry (정신과학교실)-
dc.contributor.googleauthorJung Suk Lee-
dc.contributor.googleauthorSuwon Jung-
dc.contributor.googleauthorIl Ho Park-
dc.contributor.googleauthorJae-Jin Kim-
dc.identifier.doi10.2174/1570159X13666150612230333-
dc.contributor.localIdA00870-
dc.relation.journalcodeJ03538-
dc.identifier.eissn1875-6190-
dc.identifier.pmid26630955-
dc.identifier.urlhttps://www.eurekaselect.com/article/68056-
dc.contributor.alternativeNameKim, Jae Jin-
dc.contributor.affiliatedAuthor김재진-
dc.citation.volume13-
dc.citation.number6-
dc.citation.startPage750-
dc.citation.endPage759-
dc.identifier.bibliographicCitationCURRENT NEUROPHARMACOLOGY, Vol.13(6) : 750-759, 2015-
dc.identifier.rimsid60575-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Psychiatry (정신과학교실) > 1. Journal Papers

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