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Neurotransmitters, signal transduction and second-messengers in Alzheimer's disease

1996; Wiley; Volume: 94; Issue: S165 Linguagem: Inglês

10.1111/j.1600-0404.1996.tb05869.x

1600-0404

Richard F. Cowburn, Christopher J. Fowler, Cora O’Neill,

Neurological Disorders and Treatments

Acta Neurologica ScandinavicaVolume 94, Issue S165 p. 25-32 Neurotransmitters, signal transduction and second-messengers in Alzheimer's disease R. F. Cowburn, Corresponding Author R. F. Cowburn Alzheimer's Disease Research Centre, Karolinska Institute, StockholmAlzheimer's Disease Research Centre, Karolinska Institute Department of Clinical Neuroscience and Family Medicine, Section for Geriatric Medicine, NOVUM, KFC, S-141 86 Huddinge, SwedenSearch for more papers by this authorC. J. Fowler, C. J. Fowler Department of Pharmacology, Umeå University, SwedenSearch for more papers by this authorC. O'Neill, C. O'Neill Department of Biochemistry, University College, Lee Maltings, Cork, IrelandSearch for more papers by this author R. F. Cowburn, Corresponding Author R. F. Cowburn Alzheimer's Disease Research Centre, Karolinska Institute, StockholmAlzheimer's Disease Research Centre, Karolinska Institute Department of Clinical Neuroscience and Family Medicine, Section for Geriatric Medicine, NOVUM, KFC, S-141 86 Huddinge, SwedenSearch for more papers by this authorC. J. Fowler, C. J. Fowler Department of Pharmacology, Umeå University, SwedenSearch for more papers by this authorC. O'Neill, C. O'Neill Department of Biochemistry, University College, Lee Maltings, Cork, IrelandSearch for more papers by this author First published: April 1996 https://doi.org/10.1111/j.1600-0404.1996.tb05869.xCitations: 20AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Abstract It has long been assumed that widespread changes in postsynaptic neurotransmitter receptor function are not a feature of the disrupted neurotransmission seen in the brains with Alzheimer's disease (AD). However, recent evidence from postmortem brain and fibroblast studies suggests that both the neurotransmitter receptor/G-protein-modulated adenylyl cyclase and the phosphatidylinositol hydrolysis signal transduction cascades are disrupted in AD. Such disruptions may severely limit the functional integrity of key receptor types and undermine pharmacological attempts to ameliorate disease symptomatology through neurotransmitter replacement strategies. The involvement of some signalling mechanisms in the regulation of β-amyloid precursor protein metabolism suggests also that disrupted signal transduction may exacerbate AD pathology. References 1 Young AB, Penney JB Jr. Neurotransmitter receptors in Alzheimer disease. In: RD Terry, R. Katzman, KL Bick, eds. Alzheimer disease. New York: Raven Press, 1994: 293– 303. 2 Cowburn RF, Hardy JA, Roberts PJ. Neurotransmitter deficits in Alzheimer's disease. In: DC Davies, ed. 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