0089 Chronic sleep disruption increases amyloid beta deposition and gliosis in the 5xFAD mouse model

Abstract Introduction Recent studies have found that mid-life sleep disruption is associated with the development of Alzheimer’s disease-related neuropathology, including deposition amyloid beta. Yet, mechanism connecting disruption, particularly over chronic timescales, and downstream pathology remains unclear. Methods In this study, we evaluated impact has on neuroinflammation beta plaques in 5xFAD amyloidosis mouse model. Chronic male female C57BL/6 5xFAD+ mice was performed Lafayette fragmentation cages from 10-18 weeks age. Glymphatic function assessed by measuring influx fluorescent cerebrospinal fluid tracers into brain tissue. Aquaporin-4 localization, amyloid-beta plaque deposition, markers astroglial microglial activation were immunofluorescence. Results We observed increased neuropathological outcomes littermate controls. This evident significantly gliosis, indicated increases both astrocyte (GFAP) (Iba1) expression. The glymphatic function, through tracer distribution assessment aquaporin-4 mislocalization, parallel correlated outcomes. Conclusion These findings highlight critical association between dysfunctional Alzheimer’s-related pathology. They indicate there an interaction neuroinflammation, □ deposition. Support (if any)