ReviewNeuropathology and applied neurobiology2020
Invited Review: The role of prion-like mechanisms in neurodegenerative diseases.
Review in Neuropathology and applied neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.
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.
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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
83 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Alpha-Synuclein Strain Variability in Body-First and Brain-First Synucleinopathies.Frontiers in aging neuroscience · 2022Pooled it
- TDP-43 Aggregation: The Healthy-Toxic Balance of the Prion-Like Domain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Scalable assay to identify inhibitors of prion-like propagation of protein misfolding as potential therapeutics for neurodegeneration.Protein science : a publication of the Protein Society · 2026Article
- Glucosylceramide-induced ectosomes propagate pathogenic α-synuclein in Parkinson's disease.Nature cell biology · 2026Article
- Cell type transcriptomic modules reveal shared molecular mechanisms in Alzheimer's and Parkinson's disease.GigaScience · 2026Article
- Cerebrospinal Fluid Biomarkers in Creutzfeldt-Jakob Disease: Diagnostic Value, Limitations, and Future Multi-Omics Strategies.International journal of molecular sciences · 2026Review
- One organelle to rule them all: enhancement of lysosomal activity as a therapeutic modality for protein misfolding neurodegenerative diseases.Frontiers in neuroscience · 2026Review
- Dihuang Yinzi Regulates cAMP/PKA/CREB-BDNF to Improve Synaptic Plasticity in APP/PS1 Mice: A Study Based on Brain Metabolomics.Chinese journal of integrative medicine · 2025Article
- Gene-Exercise Interactions in Amyloid Metabolism and Clearance: Implications for Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Nanoplasmonic Infrared Microarray Sensor Enabling Structural Protein Biomarker-Based Drug Screening for Neurodegenerative Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Yeast Prions: Discovery, Nature, Cellular Manipulation and Implication.Journal of microbiology and biotechnology · 2025Review
- Modulatory Effects ofAntioxidants (Basel, Switzerland) · 2025Review
- Mechanisms of Alpha-Synuclein-Seeded Aggregation in Neurons Revealed by Fluorescence Lifetime Imaging.ACS chemical neuroscience · 2025Article
- Residue-Specific Incorporation of Noncanonical Amino Acids in Auxotrophic Hosts:Chemical reviews · 2025Review
- Article
- Iatrogenic Dementia: Providing Insight into Transmissible Subtype of Alzheimer's Disease, Creutzfeldt-Jakob Disease and Cerebral Amyloid Angiopathy.Biomolecules · 2025Review
- Extracellular vesicles: new horizons in neurodegeneration.EBioMedicine · 2025Review
- Optical, contact-free assessment of brain tissue stiffness and neurodegeneration.Biomedical optics express · 2025Article
- Peripheral proteinopathy in neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Investigating the Aggregation and Prionogenic Properties of Human Cancer-Related Proteins.Molecular and cellular biology · 2025Article
23 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.
Funding
Abstract
The prototype of transmissible neurodegenerative proteinopathies is prion diseases, characterized by aggregation of abnormally folded conformers of the native prion protein. A wealth of mechanisms has been proposed to explain the conformational conversion from physiological protein into misfolded, pathological form, mode of toxicity, propagation from cell-to-cell and regional spread. There is increasing evidence that other neurodegenerative diseases, most notably Alzheimer's disease (Aβ and tau), Parkinson's disease (α-synuclein), frontotemporal dementia (TDP43, tau or FUS) and motor neurone disease (TDP43), exhibit at least some of the misfolded prion protein properties. In this review, we will discuss to what extent each of the properties of misfolded prion protein is known to occur for Aβ, tau, α-synuclein and TDP43, with particular focus on self-propagation through seeding, conformational strains, selective cellular and regional vulnerability, stability and resistance to inactivation, oligomers, toxicity and summarize the most recent literature on transmissibility of neurodegenerative disorders.
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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.