Journal
SCIENCE
Volume 363, Issue 6429, Pages 880-883Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aav2546
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Funding
- BrightFocus Foundation [A2017114F]
- Deutsche Forschungsgemeinschaft [3625/1-1]
- NIH [F32 NS089381, K08NS105929, R01NS073613, R01NS092652, P01NS074969]
- McDonnell Center for Systems Neuroscience at Washington University School of Medicine
- JPB Foundation
- Tau Consortium
- [UL1 TR000448]
- [KL2 TR000450]
- [R03 AG047999]
- [K76 AG054863]
- [P50 AG05681]
- [P01 AG26276]
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The sleep-wake cycle regulates interstitial fluid (ISF) and cerebrospinal fluid (CSF) levels of beta-amyloid (A beta) that accumulates in Alzheimer's disease (AD). Furthermore, chronic sleep deprivation (SD) increases A beta plaques. However, tau, not Ab, accumulation appears to drive AD neurodegeneration. We tested whether ISF/CSF tau and tau seeding and spreading were influenced by the sleep-wake cycle and SD. Mouse ISF tau was increased similar to 90% during normal wakefulness versus sleep and similar to 100% during SD. Human CSF tau also increased more than 50% during SD. In a tau seeding-and-spreading model, chronic SD increased tau pathology spreading. Chemogenetically driven wakefulness in mice also significantly increased both ISF A beta and tau. Thus, the sleep-wake cycle regulates ISF tau, and SD increases ISF and CSF tau as well as tau pathology spreading.
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