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- W2058878669 abstract "Fatigue is a debilitating symptom common in many neurological disorders and disease states, including Parkinson’s disease, Multiple Sclerosis and chronic fatigue syndrome. The mechanisms by which fatigue is elicited are currently unknown; however, a fatigued-state can be induced through activation of the immune system alongside other sickness behaviors. Here we describe our immune-induced animal model of fatigue using the pro-inflammatory cytokine interleukin-1 β (IL-1) in middle-aged female C57Bl/6 mice. We demonstrate reductions in voluntary wheel-running activity and general locomotor activity without the presence of other sickness behaviors including weight loss, fever, muscle ache or anhedonia. Patients experiencing fatigue report disrupted sleep–wake behavior and show lower amplitude in daily cortisol rhythms, suggesting weakness of the circadian system. We explore the effects of IL-1-induced fatigue on the coordination of the master circadian pacemaker, the suprachiasmatic nucleus (SCN), using middle-aged Per2Luc mice. We demonstrate changes in cellular rhythm coordination and alterations in response to a shifted LD cycle. These results indicate that a pro-inflammatory state might alter sleep and rhythms by direct action on SCN neurons. This work was supported by the NIH grant R21NR012845-01A1." @default.
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- W2058878669 date "2014-09-01" @default.
- W2058878669 modified "2023-09-27" @default.
- W2058878669 title "134. Deficits in circadian function in an animal model of fatigue" @default.
- W2058878669 doi "https://doi.org/10.1016/j.bbi.2014.06.154" @default.
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