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      Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle.

      Science (New York, N.Y.)

      Wakefulness, Sleep Deprivation, Sleep, Signal Transduction, metabolism, Receptors, Neuropeptide, Receptors, G-Protein-Coupled, Receptors, Cell Surface, Orexin Receptors, administration & dosage, Neuropeptides, Mice, Transgenic, Mice, Inbred C57BL, Mice, Male, Light, pharmacology, Isoquinolines, Intracellular Signaling Peptides and Proteins, Humans, Hippocampus, Female, Extracellular Fluid, Disease Models, Animal, Circadian Rhythm, Antigens, Surface, Animals, cerebrospinal fluid, Amyloid beta-Peptides, physiopathology, Alzheimer Disease, Acetamides

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          Abstract

          Amyloid-beta (Abeta) accumulation in the brain extracellular space is a hallmark of Alzheimer's disease. The factors regulating this process are only partly understood. Abeta aggregation is a concentration-dependent process that is likely responsive to changes in brain interstitial fluid (ISF) levels of Abeta. Using in vivo microdialysis in mice, we found that the amount of ISF Abeta correlated with wakefulness. The amount of ISF Abeta also significantly increased during acute sleep deprivation and during orexin infusion, but decreased with infusion of a dual orexin receptor antagonist. Chronic sleep restriction significantly increased, and a dual orexin receptor antagonist decreased, Abeta plaque formation in amyloid precursor protein transgenic mice. Thus, the sleep-wake cycle and orexin may play a role in the pathogenesis of Alzheimer's disease.

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          Author and article information

          Journal
          19779148
          2789838
          10.1126/science.1180962

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