Sleep inhibition induced by amyloid- β oligomers is mediated by the cellular prion protein.

Sleep inhibition induced by amyloid-β oligomers is mediated by the cellular prion protein. J Sleep Res. 2020 Sep 09;:e13187 Authors: Del Gallo F, Bianchi S, Bertani I, Messa M, Colombo L, Balducci C, Salmona M, Imeri L, Chiesa R Abstract Sleep is severely impaired in patients with Alzheimer's disease. Amyloid-β deposition in the brain of Alzheimer's disease patients is a key event in its pathogenesis and is associated with disrupted sleep, even before the appearance of cognitive decline. Because soluble amyloid-β oligomers are the key mediators of synaptic and cognitive dysfunction in Alzheimer's disease and impair long-term memory in rodents, the first aim of this study was to test the hypothesis that amyloid-β oligomers would directly impair sleep in mice. The cellular prion protein is a cell surface glycoprotein of uncertain function. Because cellular prion protein binds oligomeric amyloid-β with high affinity and mediates some of its neurotoxic effects, the second aim of the study was to test whether amyloid-β oligomer-induced sleep alterations were mediated by cellular prion protein. To address these aims, wild-type and cellular prion protein-deficient mice were given acute intracerebroventricular injections (on different days, at lights on) of vehicle and synthetic amyloid-β oligomers. Compared to vehicle, amyloid-β oligomers significantly reduced the amount of time spent in non-rapid eye movement sleep by wild-type mic...
Source: Journal of Sleep Research - Category: Sleep Medicine Authors: Tags: J Sleep Res Source Type: research