ArticleAutophagy2012
Activation of the macroautophagic system in scrapie-infected experimental animals and human genetic prion diseases.
Article in Autophagy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Bovine Spongiform Encephalopathy: An Integrated Review of Prion Mechanisms, Neuroanatomy, and Control.Veterinary sciences · 2026Review
- Exploring immunotherapeutic strategies for neurodegenerative diseases: a focus on Huntington's disease and Prion diseases.Acta pharmacologica Sinica · 2025Review
- Aberrant Enhanced NLRP3 Inflammasomes and Cell Pyroptosis in the Brains of Prion-Infected Rodent Models Are Largely Associated with the Proliferative Astrocytes.Molecular neurobiology · 2024Article
- Structural Variations of Prions and Prion-like Proteins Associated with Neurodegeneration.Current issues in molecular biology · 2024Review
- Diminished Neuronal ESCRT-0 Function Exacerbates AMPA Receptor Derangement and Accelerates Prion-Induced Neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Translatome profiling in fatal familial insomnia implicates TOR signaling in somatostatin neurons.Life science alliance · 2022Article
- Activation of Innate Immunity and Autophagy in Brain Tissues with Prion Disease and Degradation of Abnormal PrPs in Cells - China's Studies.China CDC weekly · 2022Review
- Therapeutic Assay with the Non-toxic C-Terminal Fragment of Tetanus Toxin (TTC) in Transgenic Murine Models of Prion Disease.Molecular neurobiology · 2021Article
- Reflections on Cerebellar Neuropathology in Classical Scrapie.Biomolecules · 2021Review
- Prion peptide-mediated calcium level alteration governs neuronal cell damage through AMPK-autophagy flux.Cell communication and signaling : CCS · 2020Article
- Impairment of autophagy in scrapie-infected transgenic mice at the clinical stage.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- An Update on Autophagy in Prion Diseases.Frontiers in bioengineering and biotechnology · 2020Review
- Dysregulation of autophagy in the central nervous system of sheep naturally infected with classical scrapie.Scientific reports · 2019Article
- Autophagy pathways in the treatment of prion diseases.Current opinion in pharmacology · 2019Review
- Cellular and Molecular Mechanisms of Prion Disease.Annual review of pathology · 2019Review
- Significant enhanced expressions of aquaporin-1, -4 and -9 in the brains of various prion diseases.Prion · 2019Article
- Lysosomal Quality Control in Prion Diseases.Molecular neurobiology · 2018Review
- What Is Our Current Understanding of PrPPathogens (Basel, Switzerland) · 2017Review
- Overexpression of PLK3 Mediates the Degradation of Abnormal Prion Proteins Dependent on Chaperone-Mediated Autophagy.Molecular neurobiology · 2017Article
- Increases of Galectin-1 and its S-nitrosylated form in the Brain Tissues of Scrapie-Infected Rodent Models and Human Prion Diseases.Molecular neurobiology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macroautophagy is an important process for removing misfolded and aggregated protein in cells, the dysfunction of which has been directly linked to an increasing number of neurodegenerative disorders. However, the details of macroautophagy in prion diseases remain obscure. Here we demonstrated that in the terminal stages of scrapie strain 263K-infected hamsters and human genetic prion diseases, the microtubule-associated protein 1 light chain 3 (LC3) was converted from the cytosolic form to the autophagosome-bound membrane form. Macroautophagy substrate sequestosome 1 (SQSTM1) and polyubiquitinated proteins were downregulated in the brains of sick individuals, indicating enhanced macroautophagic protein degradation. The levels of mechanistic target of rapamycin (MTOR) and phosphorylated MTOR (p-MTOR) were significantly decreased, which implies that this enhancement of the macroautophagic response is likely through the MTOR pathway which is a negative regulator for the initiation of macroautophagy. Dynamic assays of the autophagic system in the brains of scrapie experimental hamsters after inoculation showed that alterations of the autophagic system appeared along with the deposits of PrP(Sc) in the infected brains. Immunofluorescent assays revealed specific staining of autophagosomes in neurons that were not colocalized with deposits of PrP(Sc) in the brains of scrapie infected hamsters, however, autophagosome did colocalize with PrP(Sc) in a prion-infected cell line after treatment with bafilomycin A(1). These results suggest that activation of macroautophagy in brains is a disease-correlative phenomenon in prion diseases.
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Registered trials
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.