Bank voles are susceptible to prion strains from many different species, yet the molecular mechanisms underlying the ability of bank vole prion protein (BVPrP) to function as a universal prion acceptor remain unclear. Potential differences in molecular environments and protein interaction networks on the cell surface of brain cells may contribute to BVPrP's unusual behavior. To test this hypothesis, we generated knock-in mice that express physiological levels of BVPrP (M109 isoform) and employed mass spectrometry to compare the interactomes of mouse (Mo) PrP and BVPrP following mild in vivo crosslinking of brain tissue.
View Article and Find Full Text PDFBackground: Disturbances of the sleep-wake cycle and other circadian rhythms typically precede the age-related deficits in learning and memory, suggesting that these alterations in circadian timekeeping may contribute to the progressive cognitive decline during aging. The present study examined the role of immune cell activation and inflammation in the link between circadian rhythm dysregulation and cognitive impairment in aging.
Methods: C57Bl/6J mice were exposed to shifted light-dark (LD) cycles (12 h advance/5d) during early adulthood (from ≈ 4-6mo) or continuously to a "fixed" LD12:12 schedule.
J Lesbian Stud
January 2025
This article provides a case study of [LesPop], a police monitoring organisation that existed in London between 1984 and 1990. Drawing on archives held at Glasgow Women's Library, the article reviews the activities of LesPop and outlines its aims and objectives. We consider both its origins and its demise in the political context of Britain in the 1980s.
View Article and Find Full Text PDFProstate-specific membrane antigen (PSMA) PET was approved by the U.S. Food and Drug Administration in 2020 for the staging of newly diagnosed prostate cancer, yet rates of adoption and real-world positivity rates are unknown.
View Article and Find Full Text PDFAβ-amyloid plaques and cerebral amyloid angiopathy (CAA) in the brain are pathological hallmarks of Alzheimer's disease (AD) and vascular dementia. The spreading of Aβ amyloidosis in the brain appears to be mediated by a seeding mechanism, where preformed fibrils (called seeds) accelerate Aβ fibril formation by bypassing the rate-determining nucleation step. Several studies have demonstrated that Aβ amyloidosis can be induced in transgenic mice, producing human Aβ, by injecting Aβ-rich brain extracts (seeds) derived from transgenic mice and human AD brains.
View Article and Find Full Text PDF