ReviewInternational journal of cell biology2013
From prion diseases to prion-like propagation mechanisms of neurodegenerative diseases.
Review in International journal of cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Discovering, Integrating, and Reinterpreting the Molecular Logic of Life: From Classical Theories of Heredity to an Extended Functional Perspective on the Central Dogma.Life (Basel, Switzerland) · 2026Review
- Protein aggregation and neurodegenerative disease: Structural outlook for the novel therapeutics.Proteins · 2025Review
- The epigenetic mechanisms involved in mitochondrial dysfunction: Implication for Parkinson's disease.Brain pathology (Zurich, Switzerland) · 2022Review
- Parkinson's Disease: A Prionopathy?International journal of molecular sciences · 2021Review
- Epigenetic Regulation of Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2021Review
- Remodeling Alzheimer-amyloidosis models by seeding.Molecular neurodegeneration · 2021Review
- Extracellular Vesicles in Neurological Disorders.Sub-cellular biochemistry · 2021Article
- Challenges and Advances in Antemortem Diagnosis of Human Transmissible Spongiform Encephalopathies.Frontiers in bioengineering and biotechnology · 2020Review
- Transient multimers modulate conformer abundances of prion protein monomer through conformational selection.Scientific reports · 2019Article
- Prion-Like Mechanisms in Parkinson's Disease.Frontiers in neuroscience · 2019Review
- Low doses of bioherbicide favour prion aggregation and propagation in vivo.Scientific reports · 2018Article
- Article
- Impaired endo-lysosomal membrane integrity accelerates the seeding progression of α-synuclein aggregates.Scientific reports · 2017Article
- Types and Strains: Their Essential Role in Understanding Protein Aggregation in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2017Review
- Plasma Exosomes Spread and Cluster Around β-Amyloid Plaques in an Animal Model of Alzheimer's Disease.Frontiers in aging neuroscience · 2017Article
- Potential Pathways of Abnormal Tau and α-Synuclein Dissemination in Sporadic Alzheimer's and Parkinson's Diseases.Cold Spring Harbor perspectives in biology · 2016Review
- Human prion diseases: surgical lessons learned from iatrogenic prion transmission.Neurosurgical focus · 2016Review
- Proaggregant nuclear factor(s) trigger rapid formation of α-synuclein aggregates in apoptotic neurons.Acta neuropathologica · 2016Article
- Epigenetics and inheritance of phenotype variation in livestock.Epigenetics & chromatin · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases are fatal neurodegenerative sporadic, inherited, or acquired disorders. In humans, Creutzfeldt-Jakob disease is the most studied prion disease. In animals, the most frequent prion diseases are scrapie in sheep and goat, bovine spongiform encephalopathy in cattle, and the emerging chronic wasting disease in wild and captive deer in North America. The hallmark of prion diseases is the deposition in the brain of PrP(Sc), an abnormal β -sheet-rich form of the cellular prion protein (PrP(C)) (Prusiner 1982). According to the prion hypothesis, PrP(Sc) can trigger the autocatalytic conversion of PrP(C) into PrP(Sc), presumably in the presence of cofactors (lipids and small RNAs) that have been recently identified. In this review, we will come back to the original works that led to the discovery of prions and to the protein-only hypothesis proposed by Dr. Prusiner. We will then describe the recent reports on mammalian synthetic prions and recombinant prions that strongly support the protein-only hypothesis. The new concept of "deformed templating" regarding a new mechanism of PrP(Sc) formation and replication will be exposed. The review will end with a chapter on the prion-like propagation of other neurodegenerative disorders, such as Alzheimer's and Parkinson's disease and tauopathies.
Identifiers
What OpenQuestion holds
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.