Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.neurobiolaging.2006.06.001
Title: Disrupted muscarinic M-1 receptor signaling correlates with loss of protein kinase C activity and glutamatergic deficit in Alzheimer's disease
Authors: Tsang, Shirley WY 
Pomakian, Justine
Marshall, Gad A
Vinters, Harry V
Cummings, Jeffrey L
Chen, Christopher PL-H 
Wong, Peter T-H 
Lai, Mitchell KP 
Keywords: Science & Technology
Life Sciences & Biomedicine
Geriatrics & Gerontology
Neurosciences
Neurosciences & Neurology
muscarinic receptors
glutamate receptors
protein kinase C
Src kinase
neocortex
CHOLINERGIC HYPOTHESIS
TRANSGENIC MICE
NMDA RECEPTORS/
PKC ACTIVATORS
EXPRESSION
DEMENTIA
BINDING
PHOSPHORYLATION
BRAIN
TRANSMISSION
Issue Date: 1-Sep-2007
Publisher: ELSEVIER SCIENCE INC
Citation: Tsang, 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
Abstract: There 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.
Source Title: NEUROBIOLOGY OF AGING
URI: https://scholarbank.nus.edu.sg/handle/10635/188373
ISSN: 01974580
15581497
DOI: 10.1016/j.neurobiolaging.2006.06.001
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