Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.neurobiolaging.2006.06.001
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dc.titleDisrupted muscarinic M-1 receptor signaling correlates with loss of protein kinase C activity and glutamatergic deficit in Alzheimer's disease
dc.contributor.authorTsang, Shirley WY
dc.contributor.authorPomakian, Justine
dc.contributor.authorMarshall, Gad A
dc.contributor.authorVinters, Harry V
dc.contributor.authorCummings, Jeffrey L
dc.contributor.authorChen, Christopher PL-H
dc.contributor.authorWong, Peter T-H
dc.contributor.authorLai, Mitchell KP
dc.date.accessioned2021-04-06T01:39:50Z
dc.date.available2021-04-06T01:39:50Z
dc.date.issued2007-09-01
dc.identifier.citationTsang, Shirley WY, Pomakian, Justine, Marshall, Gad A, Vinters, Harry V, Cummings, Jeffrey L, Chen, Christopher PL-H, Wong, Peter T-H, Lai, Mitchell KP (2007-09-01). Disrupted muscarinic M-1 receptor signaling correlates with loss of protein kinase C activity and glutamatergic deficit in Alzheimer's disease. NEUROBIOLOGY OF AGING 28 (9) : 1381-1387. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neurobiolaging.2006.06.001
dc.identifier.issn01974580
dc.identifier.issn15581497
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/188373
dc.description.abstractThere are few studies on the clinical and neurochemical correlates of postsynaptic cholinergic dysfunction in Alzheimer's disease (AD). We have previously found that attenuation of guanine nucleotide-binding (G-) protein coupling to muscarinic M1 receptors in the neocortex was associated with dementia severity. The present study aims to study whether this loss of M1/G-protein coupling is related to alterations in signaling kinases and NMDA receptors. Postmortem frontal cortices of 22 AD subjects and 12 elderly controls were obtained to measure M1 receptors, M1/G-protein coupling, NMDA receptors as well as protein kinase C (PKC) and Src kinase activities. We found that the extent of M1/G-protein coupling loss was correlated with reductions in PKC activity and NMDA receptor density. In contrast, Src kinase activity was neither altered nor associated with M1/G-protein coupling. Given the well established roles of neuronal PKC signaling and NMDA receptor function in cognitive processes, our results lend further insight into the mechanisms by which postsynaptic cholinergic dysfunction may underlie the cognitive features of AD, and suggest alternative therapeutic targets to cholinergic replacement. © 2006 Elsevier Inc. All rights reserved.
dc.language.isoen
dc.publisherELSEVIER SCIENCE INC
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectGeriatrics & Gerontology
dc.subjectNeurosciences
dc.subjectNeurosciences & Neurology
dc.subjectmuscarinic receptors
dc.subjectglutamate receptors
dc.subjectprotein kinase C
dc.subjectSrc kinase
dc.subjectneocortex
dc.subjectCHOLINERGIC HYPOTHESIS
dc.subjectTRANSGENIC MICE
dc.subjectNMDA RECEPTORS/
dc.subjectPKC ACTIVATORS
dc.subjectEXPRESSION
dc.subjectDEMENTIA
dc.subjectBINDING
dc.subjectPHOSPHORYLATION
dc.subjectBRAIN
dc.subjectTRANSMISSION
dc.typeArticle
dc.date.updated2021-04-03T05:12:04Z
dc.contributor.departmentDEPT OF PHARMACOLOGY
dc.description.doi10.1016/j.neurobiolaging.2006.06.001
dc.description.sourcetitleNEUROBIOLOGY OF AGING
dc.description.volume28
dc.description.issue9
dc.description.page1381-1387
dc.description.placeUNITED KINGDOM
dc.published.statePublished
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