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Genetic variability associated with OAS1 expression in myeloid cells increases the risk of Alzheimer’s disease and severe COVID-19 outcomes

https://doi.org/10.1101/2021.03.16.435702

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Outgoing claims: the papers this work cites, builds on, or argues with.

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Diverse Brain Myeloid Expression Profiles Reveal Distinct Microglial Activation States and Aspects of Alzheimer’s Disease Not Evident in Mouse Models

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TREM2 Haplodeficiency in Mice and Humans Impairs the Microglia Barrier Function Leading to Decreased Amyloid Compaction and Severe Axonal Dystrophy

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TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer’s Disease

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Human OAS1 activation is highly dependent on both RNA sequence and context of activating RNA motifs

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Inborn errors of type I IFN immunity in patients with life-threatening COVID-19

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Autoantibodies against type I IFNs in patients with life-threatening COVID-19

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Viral Encounters with 2′,5′-Oligoadenylate Synthetase and RNase L during the Interferon Antiviral Response

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The Trem2 R47H Alzheimer’s risk variant impairs splicing and reduces Trem2 mRNA and protein in mice but not in humans

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Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2

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Normalization and variance stabilization of single-cell RNA-seq data using regularized negative binomial regression

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The age factor in Alzheimer’s disease

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Forced turnover of aged microglia induces an intermediate phenotype but does not rebalance CNS environmental cues driving priming to immune challenge

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Neurologic manifestations in hospitalized patients with COVID-19

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Long-Term Respiratory and Neurological Sequelae of COVID-19

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Local externalization of phosphatidylserine mediates developmental synaptic pruning by microglia

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Alzheimer’s Disease Variant Portal: A Catalog of Genetic Findings for Alzheimer’s Disease

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LDlinkR: An R Package for Rapidly Calculating Linkage Disequilibrium Statistics in Diverse Populations

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Canonical and Non-Canonical Aspects of JAK–STAT Signaling: Lessons from Interferons for Cytokine Responses

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Divergent Neuroinflammatory Regulation of Microglial TREM Expression and Involvement of NF-κB

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Neurologic Alterations Due to Respiratory Virus Infections

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The Spatial and Cell-Type Distribution of SARS-CoV-2 Receptor ACE2 in the Human and Mouse Brains

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OAS1 and OAS3 negatively regulate the expression of chemokines and interferon-responsive genes in human macrophages

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Fibrillar Aβ triggers microglial proteome alterations and dysfunction in Alzheimer mouse models

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Loss of TREM2 function increases amyloid seeding but reduces plaque-associated ApoE

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

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FYN, SARS-CoV-2, and IFITM3 in the neurobiology of Alzheimer's disease

inferred← citeshttps://doi.org/10.2174/0929867329666221003101548openalex-snapshot

COVID-19 and Alzheimer's Disease: Neuroinflammation, Oxidative Stress, Ferroptosis, and Mechanisms Involved

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SARS-CoV-2-Induced Type I Interferon Signaling Dysregulation in Olfactory Networks Implications for Alzheimer’s Disease

inferred← citeshttps://doi.org/10.3390/jcm15062189openalex-snapshot

Overexpression of OAS Genes in Severe COVID-19: A Cross-Sectional Study of Hospitalized Patients Infected with Delta and Omicron Variants

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Genetic Predictors of Paxlovid Treatment Response: The Role of IFNAR2, OAS1, OAS3, and ACE2 in COVID-19 Clinical Course

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