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.
|Publication status||Published - 8 Jul 2016|
|Event||International Neuropsychological Society Mid-Year Meeting - London, United Kingdom|
Duration: 6 Jul 2016 → 8 Jul 2016
|Conference||International Neuropsychological Society Mid-Year Meeting|
|Period||6/07/16 → 8/07/16|