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Individuals with Alzheimer’s Disease (AD) often experience sleep disturbances. Studies in model organisms have demonstrated ways in which sleep deprivation affects the pathophysiological pathways involved in AD pathogenesis. Studies in elderly and middle-aged individuals have shown that sleep disturbances precede the onset of cognitive impairment and dementia. However, Alzheimer’s disease pathology begins accumulating decades before symptom onset, thus the causal effect of sleep fragmentation (SF) on Alzheimer’s disease is unclear. To address this gap, genetic techniques such as Mendelian Randomization (MR) can be used to suggest causality. This study aims to disambiguate the direction of causal links between SF and AD. A genome-wide association analysis (GWAS) in adults of European ancestry from UK Biobank was conducted to identify genetic instrumental variables of SF. A two-sample MR using an inverse variance weighted approach was conducted. GWAS identified 3 risk loci for SF. MR revealed no significant causal associations in either direction.