Dual task abilities in Alzheimer’s disease due to E280A single presenilin-1 mutation

Sarah E MacPherson, Mario Parra Rodriguez, Sonia Moreno, Francisco Lopera, Sergio Della Sala

Research output: Contribution to conferencePaper

Abstract

Objective: Our previous work has demonstrated that patients with sporadicAlzheimer’s disease (AD) are impaired in their ability to performtwo tasks simultaneously compared to healthy controls, despite beingable to successfully perform the tasks alone relatively well. Yet, it remainsunclear what the earliest clinical manifestation of this dual taskcoordination deficit is. In this talk, our recent work examining dualtask abilities in individuals who are at risk of early-onset familial ADdue to an E280A presenilin-1 mutation will be discussed. The aim wasto investigate whether the dual task paradigm can differentiate betweenthose asymptomatic family members who test positive for the gene mutationand family members who test negative for the gene mutation.Participants and Methods: Twelve patients with mild AD, 25 asymptomaticcarriers and 33 non-carriers of the gene mutation were askedto perform digit recall accompanied by a secondary tracking task.Results: Despite performing well on a variety of neuropsychologicalmeasures, including episodic memory tasks, the asymptomatic carriersshow dual task decrements compared to those family members withoutthe gene mutation.
Original languageEnglish
Pages28-29
Number of pages2
Publication statusPublished - Jul 2009
EventInternational Neuropsychological Society (INS) Mid Year Meeting - Helsinki, Finland
Duration: 29 Jul 20091 Aug 2009

Conference

ConferenceInternational Neuropsychological Society (INS) Mid Year Meeting
CountryFinland
CityHelsinki
Period29/07/091/08/09

    Fingerprint

Keywords

  • alzheimer's disease
  • E280A single presenilin-1 mutation

Cite this

MacPherson, S. E., Parra Rodriguez, M., Moreno, S., Lopera, F., & Della Sala, S. (2009). Dual task abilities in Alzheimer’s disease due to E280A single presenilin-1 mutation. 28-29. Paper presented at International Neuropsychological Society (INS) Mid Year Meeting, Helsinki, Finland.