Date of Award

Fall 1-1-2025

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Public Health

First Advisor

Levy, Becca

Abstract

Background: Dementia is one of the leading causes of disability and death, and the most feared condition by older adults. Although encouraging evidence has shown that lifestyle can play a pivotal role in dementia prevention, dementia incidence is still increasing in those groups that are at most risk. A largely unexplored explanation for this phenomenon in high-risk groups is the effect of social determinants of health (SDH), a range of structural (i.e., social position, healthcare services) and psychosocial determinants (ageism, social perceptions of dementia) that can be a major modifiable driver of brain and cognitive health. Thus, by using three different methodological approaches, this thesis had the overall goal to understand how SDH influence dementia risk in those populations at greater individual (genetics) or societal (ethnicity, adverse social environment) risk of dementia and unveil new mechanisms from which addressing SDH can lead to dementia prevention. To fulfill this goal, this thesis examined for the first time what model better explain how social disadvantage interact with individual risk factor of dementia (genetic profile) to determine dementia risk (study 1), how conceptions about the causes of cognitive health (causal thinking, a new determinant of dementia) will influence the engagement in dementia prevention and risk factors in an ethnically diverse population (Indigenous and non-Indigenous people) (study 2), and if modifying these two SDH (structural determinants and conceptions about dementia prevention) can be a meaningful public health approach that will lead to improvement in dementia prevention outcomes in real-life settings (study 3). The hypotheses are that: a) genetic risk of dementia will be greatest for those at social advantage, while it will be imperceptible yet higher for those at social disadvantage (social distinction model) (study 1); b) internal causal thinking toward cognitive health will be related to better dementia prevention behaviors, but ethnic identity will determine how causal thinking impacts dementia risk (study 2); and c) modifying these two SDH (structural determinant and social conceptions of dementia) will lead to significative improvement in older adults at risk of dementia and healthcare providers’ dementia prevention outcomes in a real-life public health setting (study 3). Methods: To address the first hypothesis, a prospective observation analysis pooling data of two nationally representative studies, the Health Retirement Study (HRS) and the English Longitudinal Study of Aging (ELSA) (n: 9,849) to assess what gene-environment model better explains how social position was performed, measuring the exposure to five different SDH (education access, economic stability, healthcare quality, neighborhood environment, and social context), and how this interacts with the genetic risk profile (low, intermediate, or high risk based on APOE allele) to determine dementia risk (study one). For the second hypothesis, a mixed-method study with Indigenous (Mapuche, n: 167) and non-Indigenous (n: 245) older adults from Chile was conducted, assessing how causal thinking about cognitive problems (internal causal thinking) and trauma experiences could explain dementia prevention behaviors and risk factors in these populations (study two). To test the third hypothesis, a pragmatic randomized cluster trial was implemented assessing the efficacy of a nudge-base intervention portraying positive images about aging and Alzheimer’s disease prevention over dementia prevention outcomes of older adults at high risk of developing dementia (n: 210) and healthcare providers attending and working in senior centers, respectively. Results: As predicted by hypothesis one, the benefit and risk of APOE alleles on cognitive aging was significantly greater for those privileged to live with social advantage (ref: APOE-e3e3 at social advantage; APOE-e2 at social advantage HR:0.67, 95%CI:0.48–0.93; APOE-e4 at social advantage HR:1.68, 95%CI:1.37–2.06). However, people at social disadvantage presented the greatest dementia risk, regardless of APOE allele (ref: APOE-e3e3 at social advantage; APOE-e2 at social disadvantage HR:3.26, 95%CI:2.06–5.16; APOE-e3e3 at social disadvantage HR:3.12, 95%CI:2.47–3.95; APOE-e4 at social disadvantage HR:3.21, 95%CI:2.34–4.41). As predicted by hypothesis two, internal causal thinking about memory problems and AD were related to greater engagement in dementia prevention behaviors (memory loss B: -0.028, SE: 0.011, p: 0.015; AD B: -0.043, SE: 0.014, p: 0.002) in the combined sample. Cultural differences emerged, such that for Mapuche people a tendency to form internal attributions about memory problems led to greater engagement in dementia prevention behaviors whereas for non-Indigenous people a tendency to form internal attributions about AD led to greater engagement in dementia prevention behaviors. Furthermore, attributing memory problems to traumatic experiences (such as colonization trauma) was significantly related to greater dementia risk factors only in Mapuche people (B: 0.536, SE: 0.222, p: 0.017). Finally, as predicted by the third hypothesis, after 6 months, participants assigned to intervention (n: 101) demonstrated larger improvements in the dementia prevention behaviors score (diff of SD: 0.15, 95%CI: 0.02–0.28, p: 0.021; a 95.4% improvement compared with control group), had better cognition (memory diff: 0.24, 95%CI: 0.07 – 0.41, p: 0.031; memory-executive function diff: 0.21, 95%CI: 0.08 – 0.33, p: 0.007), a reduction in people with mild-to-moderate cognitive impairment (intervention-baseline: 70, intervention-follow-up: 67; control-baseline: 71, control-follow-up: 75; p<0.001), and increase in knowing ways to prevent dementia (intervention-baseline: 32.7%, intervention-follow-up: 61.4%, p: 0.002; control-baseline: 49.1%, control-follow-up: 50.9%, p: 0.997). In addition, in the intervention group, healthcare provider talked about dementia prevention (intervention-baseline: 9.9%, intervention-follow-up: 21.8%, p<0.001; control-baseline: 7.3%, control-follow-up: 5.5%, p: 0.973), and more people received risk factors management recommendations from healthcare providers (intervention-baseline: 53.5%, intervention-follow-up: 73.3%, p: 0.018; control-baseline: 65.5%, control-follow-up: 70.9%, p: 0.821). Conclusion: This thesis found that SDH can significantly moderate dementia risk in populations at individual and societal risk of dementia. Addressing societal and cultural determinants of dementia could bring important benefits in dementia burden reduction in the population, independently of their genetic risk, ethnic identity, or social position. Furthermore, the modifiable nature of SDH makes them a suitable target for public health to achieving long-term healthy brain and cognitive health in the population.

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