Affiliations: [a] Human Cognitive Neuroscience, Department of Psychology, University of Edinburgh, UK | [b] Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK | [c] Neuroscience Group, University of Antioquia, SIU (Sede de Investigaciones Universitaria), Antioquia, Medellin, Colombia | [d] Scottish Dementia Clinical Research Network, NHS Scotland, UK | [e] Alzheimer Scotland Dementia Research Centre, University of Edinburgh, UK | [f] UDP-INECO Foundation Core on Neuroscience (UIFCoN), Diego Portales University, Santiago, Chile
Correspondence:
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Correspondence to: Sarah E. MacPherson, Human Cognitive Neuroscience, Department of Psychology, PPLS, University of Edinburgh, 7 George Square, Edinburgh, EH8 9JZ, UK. Tel.: +44 131 650 9862; Fax: +44 131 651 3230; E-mail: [email protected].
Abstract: Patients with sporadic Alzheimer's disease (AD) are impaired in their ability to perform two tasks concurrently compared to healthy younger and older adults, despite being able to successfully perform the tasks on their own reasonably well. Dual task impairments have also been found in those individuals with an E280A presenilin-1 genetic mutation but who do not yet meet the criteria for AD. The aim of the current study is to determine whether this dual task deficit is specific to the given combination of tasks performed simultaneously or whether it reflects a general deficit in the ability to coordinate two tasks. Thirty-one carriers of the gene mutation who did not meet the criteria for AD and 38 non-carriers were asked to perform two memory tasks simultaneously. The familial AD carriers showed significant dual task decrements compared to those family members without the gene mutation. The findings support the notion that a deficit in the mechanism responsible for coordinating the performance of two tasks may be a clinical marker for the early detection of AD due to the E280A presenilin-1 gene mutation.
