ReviewClinical & developmental immunology2013
Evidence for prion-like mechanisms in several neurodegenerative diseases: potential implications for immunotherapy.
Review in Clinical & developmental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed, 36 citations in OpenAlex.
- Predicted high affinity binding of prion PRPC protein to Human Leukocyte Antigen (HLA).Journal of immunological sciences · 2026Article
- Highly sensitive chemiluminescence imaging of misfolded proteins in neurodegenerative models.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Gene-Exercise Interactions in Amyloid Metabolism and Clearance: Implications for Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Exploring immunotherapeutic strategies for neurodegenerative diseases: a focus on Huntington's disease and Prion diseases.Acta pharmacologica Sinica · 2025Review
- Structural Proteomic Profiling of Cerebrospinal Fluids to Reveal Novel Conformational Biomarkers for Alzheimer's Disease.Journal of the American Society for Mass Spectrometry · 2023Article
- Molecular Tweezers: Supramolecular Hosts with Broad-Spectrum Biological Applications.Pharmacological reviews · 2023Review
- p53 amyloid aggregation in cancer: function, mechanism, and therapy.Experimental hematology & oncology · 2022Review
- Carnosic Acid and Carnosol Display Antioxidant and Anti-Prion Properties in In Vitro and Cell-Free Models of Prion Diseases.Antioxidants (Basel, Switzerland) · 2022Article
- The Lys 280 → Gln mutation mimicking disease-linked acetylation of Lys 280 in tau extends the structural core of fibrils and modulates their catalytic properties.Protein science : a publication of the Protein Society · 2021Article
- Neuroprotective Effect of Brazilin on Amyloid β (25-35)-Induced Pathology in a Human Neuroblastoma Model.ACS omega · 2020Article
- Transcriptomic Insights into the Response of the Olfactory Bulb to Selenium Treatment in a Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2019Article
- Review
- Reduced Abundance and Subverted Functions of Proteins in Prion-Like Diseases: Gained Functions Fascinate but Lost Functions Affect Aetiology.International journal of molecular sciences · 2017Review
- Induction of PrPPrion · 2017Article
- Article
- Plasma Exosomes Spread and Cluster Around β-Amyloid Plaques in an Animal Model of Alzheimer's Disease.Frontiers in aging neuroscience · 2017Article
- Genes of susceptibility to early neurodegenerative changes in the rat retina and brain: analysis by means of congenic strains.BMC genetics · 2016Article
- Conformational selection in amyloid-based immunotherapy: Survey of crystal structures of antibody-amyloid complexes.Biochimica et biophysica acta · 2016Review
- Prion-like Mechanism in Amyotrophic Lateral Sclerosis: are Protein Aggregates the Key?Experimental neurobiology · 2015Review
- Article
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
Transmissible spongiform encephalopathies (TSEs) are fatal, untreatable neurodegenerative diseases. While the impact of TSEs on human health is relatively minor, these diseases are having a major influence on how we view, and potentially treat, other more common neurodegenerative disorders. Until recently, TSEs encapsulated a distinct category of neurodegenerative disorder, exclusive in their defining characteristic of infectivity. It now appears that similar mechanisms of self-propagation may underlie other proteinopathies such as Alzheimer's disease, Parkinson's disease, Amyotrophic lateral sclerosis, and Huntington's disease. This link is of scientific interest and potential therapeutic importance as this route of self-propagation offers conceptual support and guidance for vaccine development efforts. Specifically, the existence of a pathological, self-promoting isoform offers a rational vaccine target. Here, we review the evidence of prion-like mechanisms within a number of common neurodegenerative disorders and speculate on potential implications and opportunities for vaccine development.
Indexed as
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.