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Dual Task Abilities as a Possible Preclinical Marker of Alzheimer's Disease in Carriers of the E280A Presenilin-1 Mutation

Published online by Cambridge University Press:  02 December 2011

Sarah E. MacPherson*
Affiliation:
Department of Psychology, Human Cognitive Neuroscience and Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, United Kingdom
Mario A. Parra
Affiliation:
Department of Psychology, Human Cognitive Neuroscience and Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, United Kingdom Neuroscience Group, SIU (Sede de Investigaciones Universitaria), University of Antioquia, Medellin, Colombia
Sonia Moreno
Affiliation:
Neuroscience Group, SIU (Sede de Investigaciones Universitaria), University of Antioquia, Medellin, Colombia
Francisco Lopera
Affiliation:
Neuroscience Group, SIU (Sede de Investigaciones Universitaria), University of Antioquia, Medellin, Colombia
Sergio Della Sala
Affiliation:
Department of Psychology, Human Cognitive Neuroscience and Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, United Kingdom
*
Correspondence and reprint requests to: Sarah E. MacPherson, Department of Psychology, Human Cognitive Neuroscience, University of Edinburgh, 7 George Square, Edinburgh, United Kingdom EH8 9JZ. E-mail: sarah.macpherson@ed.ac.uk

Abstract

Previous dual task studies have demonstrated that patients with sporadic Alzheimer's disease (AD) are impaired in their ability to perform two tasks simultaneously compared with healthy controls, despite being able to successfully perform the tasks alone relatively well. Yet, it remains unclear what the earliest clinical manifestation of this dual task coordination deficit is. This study examined dual task abilities in individuals who are at risk of early-onset familial AD due to an E280A presenilin-1 mutation. Thirty-nine carriers of the gene mutation who did not meet the criteria for AD and 29 non-carrier healthy controls were asked to perform digit recall accompanied by a secondary tracking task. Individuals who were carriers of the genetic mutation demonstrated significantly higher dual task costs than healthy non-carriers. Dual task performance was found to be more sensitive to this very early stage of FAD than episodic memory measures. The findings support the notion that a deficit in the coordination mechanism of the central executive may be a pre-clinical marker for the early detection of AD due to the E280A presenilin-1 gene mutation. (JINS, 2012, 18, 234–241)

Type
Research Articles
Copyright
Copyright © The International Neuropsychological Society 2011

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Dual Task Abilities as a Possible Preclinical Marker of Alzheimer's Disease in Carriers of the E280A Presenilin-1 Mutation
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