ReviewThe American journal of pathology2008
Prion diseases: from protein to cell pathology.
Review in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Red flags for the early detection of spinal infection in back pain patients.BMC musculoskeletal disorders · 2019Pooled it
- A Drosophila model of prion disease and its metabolic changes in the brain.Animal models and experimental medicine · 2025Article
- Sleep disturbance in clinical and preclinical scrapie-infected sheep measured by polysomnography.The veterinary quarterly · 2024Article
- Present and future avenues of cell-based therapy for brain injury: The enteric nervous system as a potential cell source.Brain pathology (Zurich, Switzerland) · 2022Review
- No evidence of uptake or propagation of reindeer CWD prions in environmentally exposed sheep.Acta veterinaria Scandinavica · 2022Article
- Altered cellular localisation and expression, together with unconventional protein trafficking, of prion protein, PrPDiabetologia · 2021Article
- Tau Protein Phosphorylated at Threonine-231 is Expressed Abundantly in the Cerebellum in Prion Encephalopathies.Journal of Alzheimer's disease : JAD · 2021Article
- Extracellular Amyloid Deposits in Alzheimer's and Creutzfeldt-Jakob Disease: Similar Behavior of Different Proteins?International journal of molecular sciences · 2020Review
- Huntington disease: new insights into molecular pathogenesis and therapeutic opportunities.Nature reviews. Neurology · 2020Review
- Goats naturally devoid of PrPVeterinary research · 2020Article
- Sex differences in gene expression with galactosylceramide treatment in Cln3Δex7/8 mice.PloS one · 2020Article
- The first reported case of Creutzfeldt-Jakob disease from Nepal.Clinical case reports · 2020Article
- Brain targeting of 9c,11t-Conjugated Linoleic Acid, a natural calpain inhibitor, preserves memory and reduces Aβ and P25 accumulation in 5XFAD mice.Scientific reports · 2019Article
- Panoramic Visualization of Circulating MicroRNAs Across Neurodegenerative Diseases in Humans.Molecular neurobiology · 2019Article
- Prion Efficiently Replicates in α-Synuclein Knockout Mice.Molecular neurobiology · 2019Article
- Pressure Reveals Unique Conformational Features in Prion Protein Fibril Diversity.Scientific reports · 2019Article
- Article
- Article
- Extracellular Interactions of Alpha-Synuclein in Multiple System Atrophy.International journal of molecular sciences · 2018Review
- A new era for understanding amyloid structures and disease.Nature reviews. Molecular cell biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases or transmissible spongiform encephalopathies are fatal neurodegenerative conditions in humans and animals that originate spontaneously, genetically or by infection. Conformational change of the normal (cellular) form of prion protein (PrP c) to a pathological, disease-associated form (PrP TSE) is considered central to pathogenesis and formation of the infectious agent or prion. Neuronal damage is central to clinical manifestation of prion diseases but poorly understood. In this review, we analyze the major pathogenetic pathways that lead to tissue pathology in different forms of disease. Neuropathogenesis of prion diseases evolves in complex ways on several front lines, most but not all of which exist also in other neurodegenerative as well as infectious diseases. Whereas intracellular accumulation of PrP forms might significantly impair cell function and lead to cytopathology, mere extracellular deposition of PrP TSE is questionable as a direct cytotoxic factor. Tissue damage may result from several parallel, interacting, or subsequent pathways. Future studies should clarify the trigger(s) and sequence of these processes and whether, and which, one is dominating or decisive.
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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.