ALZHEIMER’S DISEASE: GENETIC AND SOCIO DEMOGRAPHIC INFLUENCES -A LITERATURE REVIEW

Date of Award

2025

Document Type

Thesis

Degree Name

Bachelors

Department

Natural Sciences

First Advisor

Fennie, Kristopher

Area of Concentration

Biology

Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide. Its prevalence is rapidly rising with population aging – an estimated 50 million people globally have dementia, a number projected to triple by 2050. AD is characterized pathologically by extracellular amyloid-β plaques and intracellular neurofibrillary tangles of tau protein in the brain, leading to synaptic and neuronal loss; ultimately cognitive and functional decline. This literature review examines how genetic factors and sociodemographic variables contribute to AD risk, with a focus on gene–environment interactions. A central genetic factor in late-onset AD is the apolipoprotein E (APOE) 4 allele, which confers a dose-dependent increase in risk. Rare, familial early-onset AD is caused by autosomal dominant mutations in genes like APP and PSEN1/2. Key socio demographic influences on AD include age, gender, and lifestyle factors such as physical activity, diet, education, and other aspects of cognitive maintenance. Notably, about one-third to two-fifths of AD cases worldwide may be attributable to modifiable risk factors across the person’s lifespan. Many researchers have synthesized findings from epidemiology, neuroscience, and public health literature to understand how factors like gender, age, athleticism (physical fitness), and lifestyle behaviors influence AD risk and progression. Evidence shows that a healthy lifestyle – including regular exercise, a balanced diet (e.g. Mediterranean diet), and robust cognitive and social engagement – correlates with lower AD rates and may even reduce the elevated risk presented by high-risk genotypes such as APOE E4. On the other hand, vascular and metabolic comorbidities (e.g. hypertension, diabetes, obesity), low educational attainment, and physical inactivity are associated with higher AD risk. This review finds that genetic and lifestyle factors are not independent; rather, they interact in complex ways. For example, APOE E4 carriers who maintain an active lifestyle show slower cognitive decline and less amyloid accumulation than sedentary E4 carriers. At the same time, some lifestyle interventions may have differential effects by genotype, highlighting the need for personalized prevention strategies. All in all, while age and genetics strongly influence who develops Alzheimer’s, genetic predisposition is not deterministic and engaging in protective lifestyles can enhance cognitive resilience even in at-risk populations, although important gaps remain in understanding the precise mechanisms and in translating this knowledge into effective prevention of Alzheimer’s disease.

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