ReviewFrontiers in cellular neuroscience2022
Type-I Interferons in Alzheimer's Disease and Other Tauopathies.
Review in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- The immunoproteasome in Alzheimer's disease: a dual regulator of tau pathology and microglial senescence.Inflammopharmacology · 2026Review
- Simulated wildfire smoke particulate matter elicits STING-dependent astrocyte-mediated inflammatory signaling and neurotoxicity.Neurotoxicology · 2026Article
- Lifestyle shapes preclinical social and microglial deficits in an Alzheimer's disease mouse model.Molecular psychiatry · 2026Article
- Associations between parental history of dementia and plasma markers of inflammation in a multi-ethnic middle-aged community of adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Is Alzheimer's an Autoimmune Disease?Molecular neurobiology · 2026Review
- Sustained Transcriptional Response to Lipopolysaccharide and Interleukin-4 in an Immortalized Mouse Microglial Cell Line.Molecular neurobiology · 2026Article
- Integrated Multi-Tissue Transcriptomics Reveals Antagonistic Pleiotropy in Aging and Alzheimer's Disease.Computational and structural biotechnology journal · 2026Article
- The modifier matrix: emerging roles of ubiquitin-like proteins in Alzheimer's disease.Molecular neurodegeneration advances · 2026Review
- Vascular endothelial growth factor receptor-1 (VEGFR-1) knock-down is protective against hypoxia, Aβ1-42 oligomer and Aβ1-42 fibril -induced neuronal cell death: implications in AD pathogenesis.Frontiers in neuroscience · 2026Article
- Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025Review
- Porphyromonas gingivalis outer membrane vesicles divert host innate immunity and promote inflammation via C4' monophosphorylated lipid A.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Aggregatin is a mitochondrial regulator of MAVS activation to drive innate immunity.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Identifying Alzheimer's disease-related pathways based on whole-genome sequencing data.Computational and structural biotechnology journal · 2025Article
- IFNγ preconditioning improves neuroprotection of MSC-derived vesicles on injured retinal ganglion cells by suppressing microglia activation via miRNA-dependent ribosome activity.Extracellular vesicles and circulating nucleic acids · 2025Article
- Anti-acetylated-tau immunotherapy is neuroprotective in tauopathy and brain injury.Molecular neurodegeneration · 2024Article
- Bradykinin promotes immune responses in differentiated embryonic neurospheres carrying APPCell & bioscience · 2024Article
- Human brain small extracellular vesicles contain selectively packaged, full-length mRNA.Cell reports · 2024Article
- ISGylation of DRP1 closely balances other post-translational modifications to mediate mitochondrial fission.Cell death & disease · 2024Article
- The type-I interferon response potentiates seeded tau aggregation and exacerbates tau pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Type I interferon signaling, cognition and neurodegeneration following COVID-19: update on a mechanistic pathogenetic model with implications for Alzheimer's disease.Frontiers in human neuroscience · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The detection of pathogen-associated molecular patterns can elicit the production of type-I interferons (IFNs), soluble cytokines that induce a transcriptional state inhibitory to viral replication. Signatures of type-I IFN-driven gene expression, and type-I IFNs themselves, are observed in the central nervous system during neurodegenerative diseases including Alzheimer's disease and other tauopathies, the umbrella term for diseases that feature aggregation of the cytosolic protein tau. The contribution of the type-I IFN response to pathological progression of these diseases, however, is not well-understood. The wholesale transcriptional changes that ensue from type-I IFN production can both promote protective effects and lead to damage dependent on the context and duration of the response. The type-I IFN system therefore represents a signaling pathway with a potential disease-modifying role in the progression of neurodegenerative disease. In this review we summarize the evidence for a type-I IFN signature in AD and other tauopathies and examine the role of aggregated proteins as inflammatory stimuli. We explore both the protective role of IFN against protein pathologies as well as their downstream toxic consequences, which include the exacerbation of protein pathology as a potentially destructive feed-forward loop. Given the involvement of type-I IFNs in other neurogenerative diseases, we draw comparisons with other categories of homotypic protein aggregation. Understanding how type-I IFN influences progression of AD and other tauopathies may yield important insight to neurodegeneration and identify new targets in an area currently lacking disease-modifying therapies.
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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.