A longitudinal study of dual task abilities in preclinical familial Alzheimer’s disease.

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

Research output: Contribution to conferencePaper

Abstract

Patients with sporadic Alzheimer’s disease (AD) are impaired in their ability to perform two tasks simultaneously compared to healthy younger and older adults, despite being able to perform the tasks on their own relatively well. More recently, our work has shown that dual task impairments are also found in individuals at 100% risk of developing familial AD due to an E280A presenilin-1 genetic mutation but who do not yet meet the criterion for AD. Therefore, the dual task paradigm may be a clinical marker for the early detection of AD. Objective: This study investigates the longitudinal evolution of dual tasking in preclinical AD carriers. Participants and methods: Thirty-five individuals who tested positive for the genetic mutation for early onset familial AD but who did not yet meet the criteria for AD were asked to perform the dual task paradigm, as well as episodic memory measures, at baseline and then 1 and 2 years later. Results: While the preclinical AD carriers showed a significant decline in overall dual task performance over the 2 year period, a similar significant decline was not found on the majority of the episodic memory tasks. Conclusions: These findings provide support for the notion that a deficit in the coordination mechanism of the central executive may be a clinical marker for the early detection of AD due to the E280A presenilin-1 gene mutation.
LanguageEnglish
Publication statusPublished - 8 Jul 2016

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Aptitude
Longitudinal Studies
Alzheimer Disease
Presenilin-1
Episodic Memory
Mutation
Biomarkers
Task Performance and Analysis
Young Adult

Keywords

  • Alzheimer’s disease
  • longitudinal study
  • dual task abilities

Cite this

MacPherson, Sarah E. ; Parra, Mario A. ; Moreno, Sonia ; Lopera, Francisco ; Della Sala, Sergio. / A longitudinal study of dual task abilities in preclinical familial Alzheimer’s disease.
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abstract = "Patients with sporadic Alzheimer’s disease (AD) are impaired in their ability to perform two tasks simultaneously compared to healthy younger and older adults, despite being able to perform the tasks on their own relatively well. More recently, our work has shown that dual task impairments are also found in individuals at 100{\%} risk of developing familial AD due to an E280A presenilin-1 genetic mutation but who do not yet meet the criterion for AD. Therefore, the dual task paradigm may be a clinical marker for the early detection of AD. Objective: This study investigates the longitudinal evolution of dual tasking in preclinical AD carriers. Participants and methods: Thirty-five individuals who tested positive for the genetic mutation for early onset familial AD but who did not yet meet the criteria for AD were asked to perform the dual task paradigm, as well as episodic memory measures, at baseline and then 1 and 2 years later. Results: While the preclinical AD carriers showed a significant decline in overall dual task performance over the 2 year period, a similar significant decline was not found on the majority of the episodic memory tasks. Conclusions: These findings provide support for the notion that a deficit in the coordination mechanism of the central executive may be a clinical marker for the early detection of AD due to the E280A presenilin-1 gene mutation.",
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A longitudinal study of dual task abilities in preclinical familial Alzheimer’s disease. / MacPherson, Sarah E.; Parra, Mario A.; Moreno, Sonia; Lopera, Francisco; Della Sala, Sergio.

2016.

Research output: Contribution to conferencePaper

TY - CONF

T1 - A longitudinal study of dual task abilities in preclinical familial Alzheimer’s disease.

AU - MacPherson, Sarah E.

AU - Parra, Mario A.

AU - Moreno, Sonia

AU - Lopera, Francisco

AU - Della Sala, Sergio

PY - 2016/7/8

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N2 - Patients with sporadic Alzheimer’s disease (AD) are impaired in their ability to perform two tasks simultaneously compared to healthy younger and older adults, despite being able to perform the tasks on their own relatively well. More recently, our work has shown that dual task impairments are also found in individuals at 100% risk of developing familial AD due to an E280A presenilin-1 genetic mutation but who do not yet meet the criterion for AD. Therefore, the dual task paradigm may be a clinical marker for the early detection of AD. Objective: This study investigates the longitudinal evolution of dual tasking in preclinical AD carriers. Participants and methods: Thirty-five individuals who tested positive for the genetic mutation for early onset familial AD but who did not yet meet the criteria for AD were asked to perform the dual task paradigm, as well as episodic memory measures, at baseline and then 1 and 2 years later. Results: While the preclinical AD carriers showed a significant decline in overall dual task performance over the 2 year period, a similar significant decline was not found on the majority of the episodic memory tasks. Conclusions: These findings provide support for the notion that a deficit in the coordination mechanism of the central executive may be a clinical marker for the early detection of AD due to the E280A presenilin-1 gene mutation.

AB - Patients with sporadic Alzheimer’s disease (AD) are impaired in their ability to perform two tasks simultaneously compared to healthy younger and older adults, despite being able to perform the tasks on their own relatively well. More recently, our work has shown that dual task impairments are also found in individuals at 100% risk of developing familial AD due to an E280A presenilin-1 genetic mutation but who do not yet meet the criterion for AD. Therefore, the dual task paradigm may be a clinical marker for the early detection of AD. Objective: This study investigates the longitudinal evolution of dual tasking in preclinical AD carriers. Participants and methods: Thirty-five individuals who tested positive for the genetic mutation for early onset familial AD but who did not yet meet the criteria for AD were asked to perform the dual task paradigm, as well as episodic memory measures, at baseline and then 1 and 2 years later. Results: While the preclinical AD carriers showed a significant decline in overall dual task performance over the 2 year period, a similar significant decline was not found on the majority of the episodic memory tasks. Conclusions: These findings provide support for the notion that a deficit in the coordination mechanism of the central executive may be a clinical marker for the early detection of AD due to the E280A presenilin-1 gene mutation.

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