000201200 001__ 201200
000201200 005__ 20210129215653.0
000201200 0247_ $$2doi$$a10.1093/scan/nst029
000201200 0247_ $$2ISSN$$a1749-5016
000201200 0247_ $$2ISSN$$a1749-5024
000201200 0247_ $$2WOS$$aWOS:000336489000014
000201200 0247_ $$2altmetric$$aaltmetric:1316200
000201200 0247_ $$2pmid$$apmid:23482620
000201200 037__ $$aFZJ-2015-03505
000201200 041__ $$aEnglish
000201200 082__ $$a610
000201200 1001_ $$0P:(DE-HGF)0$$aDogan, I.$$b0
000201200 245__ $$aNeural correlates of impaired emotion processing in manifest Huntington's disease
000201200 260__ $$aOxford$$bOxford Univ. Press$$c2014
000201200 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1434028032_12149
000201200 3367_ $$2DataCite$$aOutput Types/Journal article
000201200 3367_ $$00$$2EndNote$$aJournal Article
000201200 3367_ $$2BibTeX$$aARTICLE
000201200 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000201200 3367_ $$2DRIVER$$aarticle
000201200 520__ $$aThe complex phenotype of Huntington’s disease (HD) encompasses motor, psychiatric and cognitive dysfunctions, including early impairments in emotion recognition. In this first functional magnetic resonance imaging study, we investigated emotion-processing deficits in 14 manifest HD patients and matched controls. An emotion recognition task comprised short video clips displaying one of six basic facial expressions (sadness, happiness, disgust, fear, anger and neutral). Structural changes between patients and controls were assessed by means of voxel-based morphometry. Along with deficient recognition of negative emotions, patients exhibited predominantly lower neural response to stimuli of negative valences in the amygdala, hippocampus, striatum, insula, cingulate and prefrontal cortices, as well as in sensorimotor, temporal and visual areas. Most of the observed reduced activity patterns could not be explained merely by regional volume loss. Reduced activity in the thalamus during fear correlated with lower thalamic volumes. During the processing of sadness, patients exhibited enhanced amygdala and hippocampal activity along with reduced recruitment of the medial prefrontal cortex. Higher amygdala activity was related to more pronounced amygdala atrophy and disease burden. Overall, the observed emotion-related dysfunctions in the context of structural neurodegeneration suggest both disruptions of striatal-thalamo-cortical loops and potential compensation mechanism with greater disease severity in manifest HD.
000201200 536__ $$0G:(DE-HGF)POF2-332$$a332 - Imaging the Living Brain (POF2-332)$$cPOF2-332$$fPOF II$$x0
000201200 588__ $$aDataset connected to CrossRef, juser.fz-juelich.de
000201200 7001_ $$0P:(DE-HGF)0$$aSass, C.$$b1
000201200 7001_ $$0P:(DE-HGF)0$$aMirzazade, S.$$b2
000201200 7001_ $$0P:(DE-HGF)0$$aKleiman, A.$$b3
000201200 7001_ $$0P:(DE-HGF)0$$aWerner, C. J.$$b4
000201200 7001_ $$0P:(DE-HGF)0$$aPohl, A.$$b5
000201200 7001_ $$0P:(DE-HGF)0$$aSchiefer, J.$$b6
000201200 7001_ $$0P:(DE-Juel1)142495$$aBinkofski, F.$$b7
000201200 7001_ $$0P:(DE-HGF)0$$aSchulz, J. B.$$b8
000201200 7001_ $$0P:(DE-Juel1)131794$$aShah, N. J.$$b9
000201200 7001_ $$0P:(DE-Juel1)162203$$aReetz, K.$$b10$$eCorresponding Author
000201200 773__ $$0PERI:(DE-600)2236933-8$$a10.1093/scan/nst029$$gVol. 9, no. 5, p. 671 - 680$$n5$$p671 - 680$$tSocial cognitive and affective neuroscience$$v9$$x1749-5024$$y2014
000201200 8564_ $$uhttps://juser.fz-juelich.de/record/201200/files/Soc%20Cogn%20Affect%20Neurosci-2014-Dogan-671-80.pdf$$yRestricted
000201200 8564_ $$uhttps://juser.fz-juelich.de/record/201200/files/Soc%20Cogn%20Affect%20Neurosci-2014-Dogan-671-80.gif?subformat=icon$$xicon$$yRestricted
000201200 8564_ $$uhttps://juser.fz-juelich.de/record/201200/files/Soc%20Cogn%20Affect%20Neurosci-2014-Dogan-671-80.jpg?subformat=icon-1440$$xicon-1440$$yRestricted
000201200 8564_ $$uhttps://juser.fz-juelich.de/record/201200/files/Soc%20Cogn%20Affect%20Neurosci-2014-Dogan-671-80.jpg?subformat=icon-180$$xicon-180$$yRestricted
000201200 8564_ $$uhttps://juser.fz-juelich.de/record/201200/files/Soc%20Cogn%20Affect%20Neurosci-2014-Dogan-671-80.jpg?subformat=icon-640$$xicon-640$$yRestricted
000201200 8564_ $$uhttps://juser.fz-juelich.de/record/201200/files/Soc%20Cogn%20Affect%20Neurosci-2014-Dogan-671-80.pdf?subformat=pdfa$$xpdfa$$yRestricted
000201200 909CO $$ooai:juser.fz-juelich.de:201200$$pVDB
000201200 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)142495$$aForschungszentrum Jülich GmbH$$b7$$kFZJ
000201200 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131794$$aForschungszentrum Jülich GmbH$$b9$$kFZJ
000201200 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)162203$$aForschungszentrum Jülich GmbH$$b10$$kFZJ
000201200 9132_ $$0G:(DE-HGF)POF3-573$$1G:(DE-HGF)POF3-570$$2G:(DE-HGF)POF3-500$$aDE-HGF$$bKey Technologies$$lDecoding the Human Brain$$vNeuroimaging$$x0
000201200 9131_ $$0G:(DE-HGF)POF2-332$$1G:(DE-HGF)POF2-330$$2G:(DE-HGF)POF2-300$$3G:(DE-HGF)POF2$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lFunktion und Dysfunktion des Nervensystems$$vImaging the Living Brain$$x0
000201200 9141_ $$y2015
000201200 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR
000201200 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000201200 915__ $$0StatID:(DE-HGF)0130$$2StatID$$aWoS$$bSocial Sciences Citation Index
000201200 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000201200 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000201200 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000201200 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000201200 915__ $$0StatID:(DE-HGF)1020$$2StatID$$aDBCoverage$$bCurrent Contents - Social and Behavioral Sciences
000201200 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5
000201200 9201_ $$0I:(DE-Juel1)INM-4-20090406$$kINM-4$$lPhysik der Medizinischen Bildgebung$$x0
000201200 9201_ $$0I:(DE-82)080010_20140620$$kJARA-BRAIN$$lJARA-BRAIN$$x1
000201200 980__ $$ajournal
000201200 980__ $$aVDB
000201200 980__ $$aI:(DE-Juel1)INM-4-20090406
000201200 980__ $$aI:(DE-82)080010_20140620
000201200 980__ $$aUNRESTRICTED