| Abstract | Alzheimer’s Disease, a devastating neurodegenerative disease characterized by amyloid-beta plaques and neurofibrillary tangles, is the 6th leading cause of death in the U.S., and its prevalence is increasing. A common feature of Alzheimer’s is a disrupted sleep/wake cycle. 35.3% of adults in the U.S. get less than the minimum 7 hours of sleep per night recommended by the National Sleep Foundation. Interestingly, evidence suggests a bidirectional relationship between sleep loss and Alzheimer’s. We hypothesized that six weeks of sleep restriction would lead to increased amyloid-beta in the hippocampus and cognitive deficits in C57BL/6 mice. Further, we hypothesized that these effects would be exacerbated by intraperitoneal LPS administration. Chronic sleep restriction itself was associated with cognitive deficits in contextual fear conditioning, increased hippocampal amyloid-beta, and alteration in the circadian fluctuation in serum IL-1ß. Furthermore, LPS administration coupled with chronic sleep restriction led to exacerbated cognitive dysfunction. |
