Objectives: Our previous work has demonstrated that 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. However, it remains unclear what the earliest clinical manifestation of this dual task coordination deficit is. Our more recent work has focussed on dual task abilities in individuals with an E280A presenilin-1 genetic mutation which results in the development of an autosomic dominant familial AD. The aim of this study is to determine whether individuals with early onset familial forms of AD also have a selective dual task impairment and whether it is possible to differentiate between preclinical AD carriers and non-carriers of the genetic mutation using dual tasking. Methods: Patients with early onset familial AD, individuals who test positive for the genetic mutation and non-carriers of the gene mutation were asked to perform a number of dual task paradigms. Results: Both the AD patients and preclinical AD carriers showed dual task decrements compared to those family members without the gene mutation. In contrast, only the AD patients showed impairments on a variety of neuropsychological measures, including episodic memory tasks compared to the non-carriers. Conclusion: The findings support 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 - 2013|