It has been estimated that the prevalence of Alzheimer’s disease and related dementias will triple by the year 2035, unless effective interventions or treatments are found for the neurodegenerative disease. Understanding sleep as having a bidirectional relationship with Alzheimer’s disease risk and progression is a burgeoning area of investigation. Specifically, there is emerging evidence that both sleep disturbances and the APOE ε4 allele are associated with increased dementia risk. Previous research has suggested that in Alzheimer’s disease (AD), individuals carrying the APOE ε4 allele have decreased sleep quality compared to individuals without the APOE ε4 allele. This investigation aimed to determine if healthy older adults, with no cognitive impairment, with the risk allele (APOE ε4+; age 65.8±5.1; mean±SD; 37.5% female) have more sleep complaints or objective sleep disruption compared to healthy older adults, with no cognitive impairment, without the risk allele (APOE ε4-; age 64.9±5.0; 66.7% female). Within the larger Brain in Motion study (1), a subset of participants completed at home polysomnography (PSG) and actigraphy sleep assessment. Subjective sleep complaints were determined using the Pittsburg Sleep Quality Index (PSQI). Results from our study are directly relevant to an emerging research suggesting sleep as both a risk factor and symptom of neurodegenerative disease. This investigation found a significant relationship between presence of APOE ε4 allele and objective sleep disturbances measured by both actigraphy and PSG, but not subjective sleep complaints in a healthy population screened for dementia. Specifically, individuals with an APOE ε4 allele had significantly lower objective sleep efficiency measured by both PSG (73.8±17.0 vs 87.8±3.2; p < .05) and actigraphy (84.6±6.5 vs 89.7±3.3; p < .05). On the gold standard measure, PSG, there were also significant difference between APOE ε4 groups on wake after sleep onset (WASO) and total sleep time. Individuals with an APOE ε4 allele had significantly worse sleep profiles with less time spent asleep (460.3±25.4 vs 490.1±57.9; means±SD; p < .05), and significantly more WASO (108.1±73.9 vs 48.5±17.5; means±SD; p < .05). Finally, small changes in sleep architecture were observed between groups. Individuals with an APOE ε4 allele had a significantly lower percent of total sleep time spent in stage-2 NREM sleep (58.8±6.8 vs 64.2±6.4; means±SD; p < .05). There were no differences between groups in subjective sleep quality measured by the PSQI. Additionally, there were no differences between groups on arousal or awakening indices. We provide evidence that the Alzheimer’s disease risk allele APOE ε4 may be an important determinant of disrupted sleep in otherwise cognitively and physically healthy older adults. These data suggest that the impact of APOE ε4 allele on objective sleep quality may precede subjective sleep complaints in individuals at increased risk for dementia.