ArticleScientific reports2017
Differential overexpression of SERPINA3 in human prion diseases.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 59 citations in OpenAlex.
- Gpnmb defines a phagocytic state of microglia linked to cell death in prion disease mouse model.Nature communications · 2026Article
- Maternal and Fetal SERPINA3 Polymorphisms and Risk of Preeclampsia: A Dyad and Triad Based Case-Control Study.Current issues in molecular biology · 2025Article
- Functional Specificity of Astrocyte Subtypes in Alzheimer's Disease: Decoding Disease Mechanisms Through Network-based Analysis of Integrated Single-Nuclei Multi-Omic Data.Molecular neurobiology · 2025Article
- Proinflammatory transcriptomic and kinomic alterations in astrocytes derived from patients with familial Alzheimer's disease.Brain, behavior, & immunity - health · 2025Article
- Exploring SERPINA3 as a neuroinflammatory modulator in Alzheimer's disease with sex and regional brain variations.Metabolic brain disease · 2025Article
- Therapeutic Trajectories in Human Prion Diseases.Sub-cellular biochemistry · 2025Review
- Human Genetic Evidence for New Targets in Prion Diseases: Opportunities and Challenges.Sub-cellular biochemistry · 2025Review
- Cholesterol 24-hydroxylase at the choroid plexus contributes to brain immune homeostasis.Cell reports. Medicine · 2023Article
- Integrated analysis of robust sex-biased gene signatures in human brain.Biology of sex differences · 2023Article
- Strain-Dependent Morphology of Reactive Astrocytes in Human- and Animal-Vole-Adapted Prions.Biomolecules · 2023Article
- Gene expression and epigenetic markers of prion diseases.Cell and tissue research · 2023Review
- SERPINA3: Stimulator or Inhibitor of Pathological Changes.Biomedicines · 2023Review
- Urinary proteome profiles associated with cognitive decline in community elderly residents-A pilot study.Frontiers in neurology · 2023Article
- Explaining a series of models by propagating Shapley values.Nature communications · 2022Article
- Distinct translatome changes in specific neural populations precede electroencephalographic changes in prion-infected mice.PLoS pathogens · 2022Article
- Innovative Non-PrP-Targeted Drug Strategy Designed to Enhance Prion Clearance.Journal of medicinal chemistry · 2022Article
- Serpin Signatures in Prion and Alzheimer's Diseases.Molecular neurobiology · 2022Article
- Novel Exosome Biomarker Candidates for Alzheimer's Disease Unravelled Through Mass Spectrometry Analysis.Molecular neurobiology · 2022Article
- Circulating SERPINA3 improves prognostic stratification in patients with a de novo or worsened heart failure.ESC heart failure · 2021Article
- Identification and drug-induced reversion of molecular signatures of Alzheimer's disease onset and progression in AppGenome medicine · 2021Article
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Authors and funding
15 authors at 8 institutions in 5 countries.
Funding
Abstract
Prion diseases are fatal neurodegenerative disorders with sporadic, genetic or acquired etiologies. The molecular alterations leading to the onset and the spreading of these diseases are still unknown. In a previous work we identified a five-gene signature able to distinguish intracranially BSE-infected macaques from healthy ones, with SERPINA3 showing the most prominent dysregulation. We analyzed 128 suitable frontal cortex samples, from prion-affected patients (variant Creutzfeldt-Jakob disease (vCJD) n = 20, iatrogenic CJD (iCJD) n = 11, sporadic CJD (sCJD) n = 23, familial CJD (gCJD) n = 17, fatal familial insomnia (FFI) n = 9, Gerstmann-Sträussler-Scheinker syndrome (GSS)) n = 4), patients with Alzheimer disease (AD, n = 14) and age-matched controls (n = 30). Real Time-quantitative PCR was performed for SERPINA3 transcript, and ACTB, RPL19, GAPDH and B2M were used as reference genes. We report SERPINA3 to be strongly up-regulated in the brain of all human prion diseases, with only a mild up-regulation in AD. We show that this striking up-regulation, both at the mRNA and at the protein level, is present in all types of human prion diseases analyzed, although to a different extent for each specific disorder. Our data suggest that SERPINA3 may be involved in the pathogenesis and the progression of prion diseases, representing a valid tool for distinguishing different forms of these disorders in humans.
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