A mathematical model of aging-related and cortisol induced hippocampal dysfunction |
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| Authors: | Mark T McAuley Rose Anne Kenny Thomas BL Kirkwood Darren J Wilkinson Janette JL Jones and Veronica M Miller |
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| Institution: | (1) Henry Wellcome Building, Biogerontology Building, Institute for Ageing and Health, Newcastle University, NE4 6BE Newcastle upon Tyne, UK;(2) Trinity College Institute for Neuroscience, Trinity College, College Green, Dublin 2, Eire;(3) School of Mathematics & Statistics, Newcastle University, NE1 7RU Newcastle upon Tyne, UK;(4) Unilever R&D, Port Sunlight, Quarry Road East, Bebington, CH63 3JW Wirral, England,UK;(5) Neurovascular Research Unit, Institute for Ageing and Health, Newcastle General Hospital, NE46BE Newcastle upon Tyne, England, UK;(6) Wadsworth Center For Laboratories and Research, NYS Department of Health, PO Box 509, 12201-0509 Albany, NY, USA |
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| Abstract: | Background The hippocampus is essential for declarative memory synthesis and is a core pathological substrate for Alzheimer's disease
(AD), the most common aging-related dementing disease. Acute increases in plasma cortisol are associated with transient hippocampal
inhibition and retrograde amnesia, while chronic cortisol elevation is associated with hippocampal atrophy. Thus, cortisol
levels could be monitored and managed in older people, to decrease their risk of AD type hippocampal dysfunction. We generated
an in silicomodel of the chronic effects of elevated plasma cortisol on hippocampal activity and atrophy, using the systems
biology mark-up language (SBML). We further challenged the model with biologically based interventions to ascertain if cortisol
associated hippocampal dysfunction could be abrogated. |
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