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Editorial: Microglia in neuroinflammation
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Editorial: Microglia in neuroinflammation
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Journal Article
Editorial: Microglia in neuroinflammation
2023
Overview
Calreticulin has been found in human cerebrospinal fluid bound to amyloid beta (4).Reid et al.suggest that calreticulin may then serve as 1) an alarmin to recruit and activate microglia, 2) an extracellular chaperone to prevent amyloid-beta aggregation, and 3) a neuroprotectant by preventing amyloid-beta-induced, microglial-mediated neuronal loss.Karahan et al.examined the impact of the deletion of Abelson interactor family member 3 (Abi3), a candidate risk gene for Alzheimer’s disease enriched in microglia (4), in the early stages of the disease in the 5XFAD model of Alzheimer’s disease. Using this mouse strain,Church et al.showed that the protective effect of microglial depletion depends on a fully functioning CX3CR1 receptor.Reinehr et al.developed a new multifactorial glaucoma model, combining a model of spontaneous intraocular pressure with a model of autoimmune glaucoma, that developed more severe optic nerve degeneration and loss of retinal ganglion cells than its component models. Funding Participation in this Research Topic was supported by funds granted to PA by the Alzheimer’s Association (AARG-22-974642), Alfred P. Sloan Foundation (JFRASE), and MSSM/CUNY Climate Change Health Impact Interdisciplinary Research Initiative, as well as generous support by Robin Chemers Neustein; to IA by Merck KGaA (Darmstadt, Germany), the Chan Zuckerberg Initiative (CZI), the HHMI International Scholar award, European Research Council Consolidator Grant (ERC-COG) 724471-HemTree2.0, an SCA award of the Wolfson Foundation and Family Charitable Trust, the Thompson Family Foundation, an MRA Established Investigator Award (509044), the Israel Science Foundation (703/15), the Ernest and Bonnie Beutler Research Program for Excellence in Genomic Medicine, the Helen and Martin Kimmel award for innovative investigation, a NeuroMac DFG/Transregional Collaborative Research Center grant, International Progressive MS Alliance/NMSS PA-1604 08459, and an Adelis Foundation grant, and to CMC by the NIH National Institute of Allergy and Infectious Diseases to (1R01AI170938) and the Rheumatology Research Foundation (Innovative Research Award). The funders were not involved in the study design, collection, analysis, interpretation of data, the writing of this article, or the decision to submit it for publication.
