Genetic vulnerability such as APOE4 is a well-established risk factor for dementia, but its impact often becomes evident though everyday behavioral changes. Eating disturbances, measured with the Neuropsychiatric Inventory (NPI), are easily observable symptoms. These changes may signal underlying self-regulation difficulties that compromise cognition. Because executive functioning supports independence in daily life, eating disturbances may represent a pathway linking genetic risk to declines in flexibility and planning. This study examined whether appetite/eating disturbance frequency (NPI) mediates the association between APOE4 and executive functioning (TMTB) in older adults at risk of dementia, with the aim of identifying clinically relevant modifiable factors that may be addressed in clinical practice. Cross-sectional data were drawn from the Alzheimer's Disease Neuroimaging Initiative (ADNI; N = 1,729; M age = 80.04, SD = 7.8; 978 males). Diagnoses included Cognitively Normal (n = 592), Mild Cognitive Impairment (n = 977), and Dementia (n = 160). APOE4 was coded as Non-Carrier (0) or Carrier (1). Appetite/eating disturbances were measured with the NPI frequency item (range 1-4; higher scores indicate greater frequeny). Executive functioning was assessed with the Trail Making Test-B (seconds to completion). Analyses were conducted using PROCESS v4.2 (Model 4), controlling for gender and age, with 5,000 bootstrapped samples (95% CI). APOE4 carriers reported more frequent eating disturbances (B = 0.2896, p <.001). In turn, greater disturbances frequency predicted slower TMT-B performance (B = 4.2569, p < .001). The indirect effect of APOE4 on TMT-B via eating disturbances was significant (B = 1.2327, 95% CI [0.3493, 2.4522]), while the direct effect remained significant (B = 18.2194, p < .001). Beyond genetic risk, behavioral symptoms emerge as critical indicators of executive decline. These findings highlight the value of routine behavioral assessment, caregiver education, and early psychological interventions targeting eating patterns to potentially buffer cognitive deterioration in at-risk populations.