ReviewAnnual review of neuroscience2015
Neurodegenerative diseases: expanding the prion concept.
Review in Annual review of neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
186 citing papers in PubMed, 2 syntheses or guidelines pooled it, 353 citations in OpenAlex.
- Alpha-Synuclein Strain Variability in Body-First and Brain-First Synucleinopathies.Frontiers in aging neuroscience · 2022Pooled it
- The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion.Frontiers in neuroscience · 2021Pooled it
- Alzheimer's Disease Accelerates Cerebral Atrophy by Over a Decade Compared to Healthy Aging.Annals of biomedical engineering · 2026Article
- Review
- The default mode network exhibits circuit-specific selective vulnerability despite widespread amyloid burden in an animal model of Alzheimer's disease.Nature communications · 2026Article
- Tau physiology and pathology: impacts on cellular structures and neurodegenerative diseases.Inflammopharmacology · 2026Review
- Nanoscale morphological and structural analysis of round and donut oligomers formed by C-terminal domain of TDP-43.Physical chemistry chemical physics : PCCP · 2026Article
- Cellular prion protein and its derived peptides: multifaceted roles in neurodegenerative diseases and potential as biomarkers.Cell & bioscience · 2026Review
- Digital seed amplification assay for TDP-43 aggregate quantification in CSF.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Human Brain Contusions Contain Pathogenic Transmissible Species that Induce Progressive Cognitive Decline and Tau Pathology in Mice.Annals of neurology · 2026Article
- Dietary Bioactives in Alzheimer's Disease: A Critical Appraisal of Clinical Trials and Future Nutritional Strategies.Nutrients · 2026Review
- Zooming into Disease at the Nanoscale: High-Speed Atomic Force Microscopy in Biomedical Discovery.ACS nano · 2026Review
- Elucidation of Molecular Mechanisms of Lipid-Altered Cytotoxicity of TDP-43 Fibrils.ACS chemical neuroscience · 2026Article
- The gut-brain axis in Alzheimer's disease: early detection, microbial metabolites, mechanisms, and therapeutic opportunities.Frontiers in molecular biosciences · 2026Review
- Neurodegeneration as Ecosystem Failure: A New Paradigm for Prevention and Treatment.International journal of molecular sciences · 2025Review
- Digital seed amplification assay for TDP-43 aggregate quantification in CSF.medRxiv : the preprint server for health sciences · 2025Article
- Impact of Lysine Acetylation Mutations on the Structure of Full-Length Tau Fibrils.ACS chemical neuroscience · 2025Article
- Personalised regional modelling predicts tau progression in the human brain.PLoS biology · 2025Article
- Transplantation of human glial cells into murine brains: A systematic review of efficacy and safety in neurodegenerative disorders.Current journal of neurology · 2025Review
- Modeling Necroptotic and Pyroptotic Signaling inBiomolecules · 2025Review
126 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 2 countries.
Funding
Abstract
The prion paradigm has emerged as a unifying molecular principle for the pathogenesis of many age-related neurodegenerative diseases. This paradigm holds that a fundamental cause of specific disorders is the misfolding and seeded aggregation of certain proteins. The concept arose from the discovery that devastating brain diseases called spongiform encephalopathies are transmissible to new hosts by agents consisting solely of a misfolded protein, now known as the prion protein. Accordingly, "prion" was defined as a "proteinaceous infectious particle." As the concept has expanded to include other diseases, many of which are not infectious by any conventional definition, the designation of prions as infectious agents has become problematic. We propose to define prions as "proteinaceous nucleating particles" to highlight the molecular action of the agents, lessen unwarranted apprehension about the transmissibility of noninfectious proteopathies, and promote the wider acceptance of this revolutionary paradigm by the biomedical community.
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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.