Irina F. Roschina

Background. Aging is associated with decline in various cognitive functions, including task switching – the ability to shift quickly between tasks and mindsets. Previous research has shown that older adults exhibit less efficient task switching. Mathematical modeling of cognitive processes involved in switching between tasks may shed light on the sources of switching inefficiency in normal and pathological cognitive aging.

Objective. To investigate possible sources of task-switching decline in normal and pathological (mild cognitive impairment, MCI) cognitive aging using the Diffusion Model (DM). 

Design. 57 young adults, 34 healthy older participants, and 5 MCI-diagnosed older participants performed the commonly used Number-Letter switching task. Reaction times (RT) and accuracy were measured and Diffusion Models were fitted to individual reaction time distribution to obtain parameters characterizing processes involved in task switching: active, controlled task-set reconfiguration; passive, automatic task-set inertia; and response caution. 

Results. Older age and MCI-pathology-related effects on switching efficiency were found for RT and, partly, for accuracy. After controlling for possible age differences between the two older groups, active processes of task-set reconfiguration had a clear MCI-related deficit, while passive, automatic task-set inertia components only exhibited a general effect of aging (pathological or not). Response caution was only related to older age, with no MCI effect.

Conclusion. Effortful task-set reconfiguration is sensitive to both age and MCI pathology, while passive processes of task-set inertia dissipation is only subject to age changes. The results support the idea of different dynamics of controlled and automatic cognitive processes in normal and pathological (MCI) aging.

A major risk factor for late-onset Alzheimer’s type dementia (DAT) is the carriage of the ε4 allele of the apolipoprotein E (ApoE) gene. Identifying cognitive deficits in healthy ApoE-ε4 carriers is valuable in order to develop interventions to prevent them from developing DAT. Existing evidence about cognitive deficits in the domains of episodic memory and cognitive control specific to ApoE-ε4 is contradictory.

The objective of our research was to assess episodic memory and cognitive control in healthy ApoE-ε4 carriers.

Cognitively healthy ApoE-ε4 carriers (13 ε4/ε4 heterozygotes) and noncarriers (22 ε3/ε3 homozygotes), who were matched on age and family history of DAT, were compared on episodic-memory and cognitive-control tasks. Episodic-memory tasks were verbal and visual recognition tasks with a systematic variation of distractor-to-target similarity. Executive functions were assessed by a task for updating working memory, an inhibition task, and a switching task. Working-memory capacity was also assessed.

The results showed that executive functions were generally not impaired in the carriers, but carriers showed a specific increase in accuracy-related switch costs. Workingmemory capacity was not reduced in the carriers. In the domain of episodic memory, the carriers were found to make more errors with phonetic distractors in the verbal episodicmemory task. They also tended to make more errors with visually dissimilar distractors in the visual episodic-memory task.

The results are indicative of an episodic-memory deficit specific to the carriage of ApoE-ε4. This deficit may be driven either by deficits in storage or by deficits in the encoding of the to-be-remembered material. Contradictory results concerning the presence of an episodic-memory deficit obtained in previous studies may stem from small effect sizes, the use of specific materials, and the employment of attention-intensive encoding strategies. The carriers also showed a switching deficit that possibly is related to difficulty in retrieving task rules from episodic memory. Existing empirical contradictions concerning the presence of an executive deficit in carriers may in part depend on the extent to which tasks used to assess an executive deficit draw on the switching function. In this study, there was no general executive deficit in the carriers of ApoE-ε4.