Please use this identifier to cite or link to this item: https://doi.org/10.1007/s00702-013-1067-0
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dc.titleDecreased immunoreactivities of neocortical AMPA receptor subunits correlate with motor disability in Lewy body dementias
dc.contributor.authorMohamed, Nur-Ezan
dc.contributor.authorHowlett, David R
dc.contributor.authorMa, Lu
dc.contributor.authorFrancis, Paul T
dc.contributor.authorAarsland, Dag
dc.contributor.authorBallard, Clive G
dc.contributor.authorMcKeith, Ian G
dc.contributor.authorChen, Christopher P
dc.contributor.authorLai, Mitchell KP
dc.date.accessioned2021-04-06T06:02:56Z
dc.date.available2021-04-06T06:02:56Z
dc.date.issued2014-01-01
dc.identifier.citationMohamed, Nur-Ezan, Howlett, David R, Ma, Lu, Francis, Paul T, Aarsland, Dag, Ballard, Clive G, McKeith, Ian G, Chen, Christopher P, Lai, Mitchell KP (2014-01-01). Decreased immunoreactivities of neocortical AMPA receptor subunits correlate with motor disability in Lewy body dementias. JOURNAL OF NEURAL TRANSMISSION 121 (1) : 71-78. ScholarBank@NUS Repository. https://doi.org/10.1007/s00702-013-1067-0
dc.identifier.issn03009564
dc.identifier.issn14351463
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/188424
dc.description.abstractDementia with Lewy bodies and Parkinson's disease dementia are different clinical phenotypes of Lewy body dementias differentiated by the temporal relationship between parkinsonism and dementia onset. At present, it is unclear whether the glutamatergic system is affected in these disorders. In this study, we measured α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor GluA subunits in the postmortem neocortex of a cohort of prospectively studied Lewy body dementia cases, as well as age-matched controls by immunoblotting. We found losses of GluA2/3/4 immunoreactivities in Lewy body dementias which correlated with higher pre-death Hoehn and Yahr scores and with longer Parkinson's disease duration before dementia onset, but not with dementia severity, cortical Lewy body burden, or amyloid plaque and neurofibrillary tangle burden. Our study suggests that GluA2/3/4 losses may be a neurochemical marker of motor disability in Lewy body dementias. © 2013 Springer-Verlag Wien.
dc.language.isoen
dc.publisherSPRINGER WIEN
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectClinical Neurology
dc.subjectNeurosciences
dc.subjectNeurosciences & Neurology
dc.subjectAMPA receptors
dc.subjectLewy body dementia
dc.subjectNeocortex
dc.subjectMotor function
dc.subjectGlutamatergic system
dc.subjectPARKINSONS-DISEASE
dc.subjectALZHEIMERS-DISEASE
dc.subjectGLUTAMATE RECEPTORS
dc.subjectSYNAPTIC PLASTICITY
dc.subjectVASCULAR DEMENTIA
dc.subjectDOPAMINE
dc.subjectCONSORTIUM
dc.subjectBODIES
dc.subjectNEURONS
dc.subjectDIAGNOSIS
dc.typeArticle
dc.date.updated2021-04-03T05:25:01Z
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1007/s00702-013-1067-0
dc.description.sourcetitleJOURNAL OF NEURAL TRANSMISSION
dc.description.volume121
dc.description.issue1
dc.description.page71-78
dc.description.placeAUSTRIA
dc.published.statePublished
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