ArticleBrain : a journal of neurology2021
A genetic link between risk for Alzheimer's disease and severe COVID-19 outcomes via the OAS1 gene.
Article in Brain : a journal of neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 2 of them syntheses that pooled it.
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Who cites it
71 citing papers in PubMed, 2 syntheses or guidelines pooled it, 110 citations in OpenAlex.
- Pooled it
- Mendelian randomization and genetic colocalization infer the effects of the multi-tissue proteome on 211 complex disease-related phenotypes.Genome medicine · 2022Pooled it
- Genetic drivers of progression in Alzheimer's disease are distinct from disease risk.Alzheimer's research & therapy · 2026Article
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- Can we refute a role for infections in Alzheimer's disease pathogenesis?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Roles of Reactive Oxygen Species in Relationships Between Viral Infections and Alzheimer's Disease and Related Dementia.Antioxidants (Basel, Switzerland) · 2026Review
- Identification of Shared Gene Signatures Associated with Alzheimer's Disease and COVID-19 through Bioinformatics Analysis.Combinatorial chemistry & high throughput screening · 2026Article
- Regulators of interferon-responsive microglia uncovered by Genome-wide CRISPRi screening.NPJ dementia · 2026Article
- MiR-34a deficiency enhances nucleic acid sensing and type I IFN signaling in a mouse model of Alzheimer's disease.Frontiers in immunology · 2026Article
- Genetic drivers of progression in Alzheimer's disease are distinct from disease risk.medRxiv : the preprint server for health sciences · 2025Article
- The expression signature, prognostic significance and immune cell infiltration of the OAS gene family in gastric cancer.Scientific reports · 2025Article
- Human microglia differentially respond to β-amyloid, tau, and combined Alzheimer's disease pathologies in vivo.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Expression of SARS-CoV-2 entry receptor ACE2 in human brain and its association with Alzheimer's disease and COVID-19.Molecular psychiatry · 2025Review
- Chronic alcohol exposure during young adulthood attenuates microglial reactivity and downstream immune response pathways in a mouse model of tauopathy later in life.Alcohol, clinical & experimental research · 2025Article
- Cell-Autonomous Immunity: From Cytosolic Sensing to Self-Defense.International journal of molecular sciences · 2025Review
- Genetic Predictors of Paxlovid Treatment Response: The Role of IFNAR2, OAS1, OAS3, and ACE2 in COVID-19 Clinical Course.Journal of personalized medicine · 2025Article
- Identifying risk factors and predicting long COVID in a Spanish cohort.Scientific reports · 2025Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 7 institutions in 2 countries.
Funding
Abstract
Recently, we reported oligoadenylate synthetase 1 (OAS1) contributed to the risk of Alzheimer's disease, by its enrichment in transcriptional networks expressed by microglia. However, the function of OAS1 within microglia was not known. Using genotyping from 1313 individuals with sporadic Alzheimer's disease and 1234 control individuals, we confirm the OAS1 variant, rs1131454, is associated with increased risk for Alzheimer's disease. The same OAS1 locus has been recently associated with severe coronavirus disease 2019 (COVID-19) outcomes, linking risk for both diseases. The single nucleotide polymorphisms rs1131454(A) and rs4766676(T) are associated with Alzheimer's disease, and rs10735079(A) and rs6489867(T) are associated with severe COVID-19, where the risk alleles are linked with decreased OAS1 expression. Analysing single-cell RNA-sequencing data of myeloid cells from Alzheimer's disease and COVID-19 patients, we identify co-expression networks containing interferon (IFN)-responsive genes, including OAS1, which are significantly upregulated with age and both diseases. In human induced pluripotent stem cell-derived microglia with lowered OAS1 expression, we show exaggerated production of TNF-α with IFN-γ stimulation, indicating OAS1 is required to limit the pro-inflammatory response of myeloid cells. Collectively, our data support a link between genetic risk for Alzheimer's disease and susceptibility to critical illness with COVID-19 centred on OAS1, a finding with potential implications for future treatments of Alzheimer's disease and COVID-19, and development of biomarkers to track disease progression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.