Hiu Chuen Lok

Introduction Alzheimer’s disease (AD) is the most common neurodegenerative disease, and its main clinical manifestations are cognitive impairment and progressive decline of memory ability (GBD 2016 Neurology Collaborators, 2019). The main pathology of AD includes amyloid (Aβ) plaque deposition and neurofibrillary tangles (NFTs) formed by hyperphosphorylation of Tau (Hodson, 2018; Scheltens et al., 2021). With the acceleration of population aging, the prevalence of AD has increased dramatically.

Michael S. Petronek1*, Khaliunaa Bayanbold1, Koffi Amegble2, Ann M. Tomanek-Chalkley1, Bryan G. Allen1, Douglas R. Spitz1 and Charvann K. Bailey2* 1Department of Radiation Oncology, Division of Free Radical and Radiation Biology, University of Iowa, Iowa City, IA, United States 2Department of Biology, Grinnell College, Grinnell, IA, United States A distinctive feature of cancer is the upregulation of sirtuin proteins.

NO-induced 59Fe Release from Activated RAW 264.7 and J744 Macrophages Is Markedly Reduced by Mrp1 Silencing To evaluate the role of MRP1 in 59Fe release from activated macrophages, we used the RAW 264.7 and J774 cell types, which become activated and generate NO via iNOS after incubation with LPS (100 ng/ml) and IFNγ (50 units/ml) (Fig. 1, A–L) (48–52).