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.