Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.jns.2009.08.066
DC FieldValue
dc.titleA serotoninergic basis for hyperphagic eating changes in Alzheimer's disease
dc.contributor.authorTsang, Shirley W
dc.contributor.authorKeene, Janet
dc.contributor.authorHope, Tony
dc.contributor.authorSpence, Ian
dc.contributor.authorFrancis, Paul T
dc.contributor.authorWong, Peter T-H
dc.contributor.authorChen, Christopher P
dc.contributor.authorLai, Mitchell K
dc.date.accessioned2021-04-06T03:04:26Z
dc.date.available2021-04-06T03:04:26Z
dc.date.issued2010-01-15
dc.identifier.citationTsang, Shirley W, Keene, Janet, Hope, Tony, Spence, Ian, Francis, Paul T, Wong, Peter T-H, Chen, Christopher P, Lai, Mitchell K (2010-01-15). A serotoninergic basis for hyperphagic eating changes in Alzheimer's disease. JOURNAL OF THE NEUROLOGICAL SCIENCES 288 (1-Feb) : 151-155. ScholarBank@NUS Repository. https://doi.org/10.1016/j.jns.2009.08.066
dc.identifier.issn0022510X
dc.identifier.issn18785883
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/188384
dc.description.abstractHyperphagia and associated eating changes occur frequently in Alzheimer's disease (AD) and lead to considerable morbidity. However, the neurochemical basis for these neuropsychiatric behaviours is at present unclear. In this study, we measured serotonin transporters, 5-HT1A, 5-HT2A, and 5-HT4 receptors using radioligand binding assays in the postmortem temporal cortex of a cohort of controls and AD patients longitudinally assessed for hyperphagia. We found significant decreases in 5-HT4 receptor densities in the hyperphagic, but not normophagic, AD group. Our data suggest that 5-HT4 receptor deficits may be a specific neurochemical correlate of hyperphagia, and point to the potential pharmacotherapeutic utility of 5-HT4 agonists for these behaviours in AD. © 2009 Elsevier B.V. All rights reserved.
dc.language.isoen
dc.publisherELSEVIER SCIENCE BV
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectClinical Neurology
dc.subjectNeurosciences
dc.subjectNeurosciences & Neurology
dc.subjectAlzheimer's disease
dc.subjectDementia
dc.subjectHyperphagia
dc.subjectSerotonin receptor
dc.subjectSerotonin transporter
dc.subjectNeocortex
dc.subjectPOSITRON-EMISSION-TOMOGRAPHY
dc.subject5-HT1A RECEPTOR-BINDING
dc.subjectFRONTOTEMPORAL DEMENTIA
dc.subjectBEHAVIORAL-CHANGES
dc.subjectCOGNITIVE DECLINE
dc.subjectANOREXIA-NERVOSA
dc.subjectFEEDING-BEHAVIOR
dc.subjectNATURAL-HISTORY
dc.subjectBULIMIA-NERVOSA
dc.subjectTEMPORAL-LOBE
dc.typeArticle
dc.date.updated2021-04-03T05:17:14Z
dc.contributor.departmentDEPT OF PHARMACOLOGY
dc.description.doi10.1016/j.jns.2009.08.066
dc.description.sourcetitleJOURNAL OF THE NEUROLOGICAL SCIENCES
dc.description.volume288
dc.description.issue1-Feb
dc.description.page151-155
dc.description.placeNETHERLANDS
dc.published.statePublished
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