OBSTRUCTIVE SLEEP APNEA SYNDROME (OSAS) IS A SLEEP DISORDER, INVOLVING THE REPETITIVE OCCURRENCE OF PARTIAL (HYPOPNEA) OR COMPLETE (apnea) interruptions of airflow during sleep. The severity of OSAS is determined by the frequency of obstructive respiratory events, expressed as the apnea-hypopnea index (AHI). OSAS patients display daytime sleepiness, mood disturbances, and cognitive impairment.1 Obstructive sleep apnea is closely associated with obesity and aging.2 OSAS has a high cardiovascular comorbidity, and some authors see a potential link between OSAS and dementia.3 Apolipoprotein E (ApoE) genotype epsilon 4 is a well-known risk factor for Alzheimer disease.4 Associations between ApoE genotype epsilon 4 subtype and vascular dementia have been demonstrated.5,6 The Wisconsin Sleep Cohort Study showed a significantly higher probability of moderate to severe (AHI≥15) sleep disordered breathing among participants with ApoE genotype epsilon 4 (12%), independent of age, sex, BMI, and ethnicity than in subjects with an AHI<15 (7%). The mean AHI among participants with ApoE genotype epsilon 4 (28% of the cohort) was significantly higher (6.5 vs. 4.8; P = .01) than in subjects without this genotype.7 In another population-based study, the presence of ApoE genotype epsilon 4 was associated with an increased odds ratio for OSAS.8 Daytime impairment in OSAS patients has long been suspected to be a consequence of underlying brain dysfunction and/or damage. This has led to increasing research, particularly using neuroimaging in OSAS patients, in order to investigate possible neurodegenerative and metabolic aspects. But we found no comprehensive review summarizing the results of neuropsychological daytime impairment and linking them to recent neuroimaging studies and research on cerebrovascular impairment in OSAS patients. Therefore we have attempted to make a contribution to filling this gap.