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Locus of Control (LoC) is the degree to which people believe that they, as opposed to external forces, have control over the outcome of events in their lives. An ‘external’ LoC supports a belief that one is not in control of life events (e.g. successes and failures); an ‘internal’ LoC supports the belief that life events are due to one’s own efforts. LoC has been adversely associated with many psychological and physical health outcomes over the previous two decades, with a general view that greater externality is associated with poorer health outcomes such as obesity and depression. However, few studies have examined whether it is related to cognitive function in adulthood. Given treatments for cognitive decline are sparse and very few modifiable risk factors have been identified to inform prevention strategies, we examined the effect of LoC on cognitive function in adulthood.

In 1178 women from the Avon Longitudinal Study of Parents And Children, we examined the association between LoC, and change in LoC over almost 20 years, with cognitive function in midlife. LoC was prospectively measured at mean ages 30 and 48 years, using the widely validated Nowicki-Strickland scale. Cognitive function was examined at mean age 51 years.

Greater externality was consistently associated with lower cognitive function. For example, women classified as being external at mean age 48 years had, on average, a 0.18 lower cognitive function score (95% CI: 0.11 to 0.25) than the group classified as being internal (p<0.001). Participants who changed from external to internal over time, on average, had better cognitive function than those who remained external or changed to become external.

In summary, an external LoC is likely to be detrimental to cognitive function. Interventions to increase internality may help to minimise the adverse consequences on cognitive health later in life. Further studies should try to elucidate the mechanisms through which externality may be detrimental to cognitive performance to highlight additional potential interventions.

Older adults seeking assessment for forgetfulness, absent-mindedness, and difficulty completing complex tasks, are usually worried they are exhibiting early signs of dementia. Careful documentation of symptom history, however, indicates that some represent undetected attention-deficit/hyperactivity disorder (ADHD), which may only manifest fully in later life (e.g., following changes to previously effective internal or external structures) and thus mimic a late-onset neurodegenerative syndrome. On the other hand, emerging research suggests ADHD may actually increase dementia risk. Two studies were undertaken to elucidate whether ADHD is more likely to be a phenotypic mimic (vs. a prodrome) of neurodegeneration.

A first study aimed to quantify the overlapping and unique features of ADHD and mild cognitive impairment (MCI, presumed to be a true dementia prodrome). Forty older adults with ADHD, 29 with MCI and 37 controls underwent neuropsychological assessment. A subsample (n=80) also underwent structural neuroimaging. Analyses revealed memory impairments in both patient groups, which reflected a storage deficit in MCI (supported by reduced hippocampal volumes) and an encoding deficit in ADHD (supported by frontal-lobe cortical thinning). Semantic retrieval was uniquely impaired in MCI.

A second study constituted a retrospective chart review of six older adults with ADHD with repeated clinical neuropsychological assessment across 5 to 21 years. Longitudinal performance was inspected to determine the extent of cognitive change. Overall, most participants performed normally on measures of attention, language, speeded switching and working memory. Four participants had at least one time point at which memory was impaired, but no participants’ abilities declined notably across time. Visuo-constructional abilities and cognitive flexibility were borderline to impaired in most participants across all time points but showed no significant decline. There were no obvious relationships between fluctuations in cognitive performance and depressive symptoms.

In conclusion, both ADHD and MCI show important dementia-like features (i.e., memory deficits), which may cause ADHD to present as a pseudodementia syndrome. Overall different cognitive profiles (i.e., unique language and memory processes deficits in MCI) and neuroimaging profiles (i.e., frontal-lobe thinning in ADHD), along with generally stable cognition longitudinally in ADHD, tentatively suggest that it is not associated with neurodegeneration but rather mimicking its phenotypical presentation in some respects.

BACKGROUND: It is well-documented that African Americans are at elevated risk for cognitive impairment and dementia in late life, but reasons for the racial disparity remain underexplained. Stress processes have been linked to premature age-related morbidity, including cognitive impairment and risk for Alzheimer’s disease and related dementias (ADRD). Disproportionately high exposure to stressors among minoritized populations plausibly contributes to social disparities in cognitive aging.

OBJECTIVE: We examined the relationship between stressful life events and cognitive decline among African American and White participants enrolled in the Wisconsin Registry for Alzheimer’s Prevention (WRAP). METHODS: Linear mixed models including demographic, literacy, and health-related covariates were used to estimate (1) relationships between a life event index score and decline in cognitive test performance in two domains of executive function (Speed & Flexibility, Working Memory) and one domain of episodic memory (Verbal Learning & Memory) among 1,241 WRAP enrollees, stratified by race, and (2) contributions of stressful life events to racial differences in cognition within the full sample.

RESULTS: African Americans (N=50) reported more stressful life events than Whites (N=1,191). Higher stress scores associated with poorer Speed & Flexibility performance in both groups, though not with declines across time, and partially explained racial differentials in this domain. Among African Americans only, stressor exposure also associated with age-related decline in Verbal Learning & Memory. Stressor-cognition relationships were robust to adjustment for literacy and health-related variables.

CONCLUSIONS: Our findings are congruent with literature demonstrating that conditions of structural and interpersonal racism associate with stress exposure across the life course. In this study, greater lifetime stress predicted poorer later-life cognition, and, in a small sample of African Americans, faster declines in a key domain of episodic memory. This preliminary work suggests that future work in large minority aging cohorts should explore stress as an important source of modifiable, socially-rooted risk for impairment and ADRD in African Americans.