ReviewAnnual review of genetics2013
Biology and genetics of prions causing neurodegeneration.
Review in Annual review of genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 247 papers, 1 of them a synthesis 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
247 citing papers in PubMed, 1 synthesis or guideline pooled it, 444 citations in OpenAlex.
- The Role of Protein Misfolding and Tau Oligomers (TauOs) in Alzheimer's Disease (AD).International journal of molecular sciences · 2019Pooled it
- A Neuronal Cell Line Model for Studying Camel Prions.Pathogens (Basel, Switzerland) · 2026Article
- Bovine Spongiform Encephalopathy: An Integrated Review of Prion Mechanisms, Neuroanatomy, and Control.Veterinary sciences · 2026Review
- Selection for Function in Complex Distributed Pathological Systems.Evolutionary applications · 2026Article
- Computational Exploration of Phospholipid Alterations in a Human Neuroblastoma Cell Model Exposed to Amyloid-Beta.Advances in experimental medicine and biology · 2026Article
- Article
- Physics of Protein Aggregation in Normal and Accelerated Brain Aging.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Inducers and modulators of protein aggregation in Alzheimer's disease - Critical tools for understanding the foundations of aggregate structures.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Chlorogenic Acid Enhances the Chaperone Potential of BSA at Physiological Concentrations on Model Protein Cytochrome c.Cell biochemistry and biophysics · 2025Article
- A Review of CAC-717, a Disinfectant Containing Calcium Hydrogen Carbonate Mesoscopic Crystals.Microorganisms · 2025Review
- Enhanced secretion of the amyotrophic lateral sclerosis ALS-associated misfolded TDP-43 mediated by the ER-ubiquitin specific peptidase USP19.Cellular and molecular life sciences : CMLS · 2025Article
- Peripheral proteinopathy in neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Seeding activity of skin misfolded tau as a biomarker for tauopathies.Molecular neurodegeneration · 2024Article
- Degradation and/or Dissociation of Neurodegenerative Disease-Related Factor Amyloid-β by a Suspension Containing Calcium Hydrogen Carbonate Mesoscopic Crystals.International journal of molecular sciences · 2024Article
- Osmotic stress induces formation of both liquid condensates and amyloids by a yeast prion domain.The Journal of biological chemistry · 2024Article
- Enteric Nervous System and Its Relationship with Neurological Diseases.Journal of clinical medicine · 2024Article
- The prion principle and Alzheimer's disease.Science (New York, N.Y.) · 2024Article
- The Role of α-Synuclein in Etiology of Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- The integrated stress response in brain diseases: A double-edged sword for proteostasis and synapses.Current opinion in neurobiology · 2024Review
- Tissue-specific landscape of protein aggregation and quality control in an aging vertebrate.Developmental cell · 2024Article
187 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
1 author at 1 institution in 1 country.
Funding
Abstract
Prions are proteins that acquire alternative conformations that become self-propagating. Transformation of proteins into prions is generally accompanied by an increase in β-sheet structure and a propensity to aggregate into oligomers. Some prions are beneficial and perform cellular functions, whereas others cause neurodegeneration. In mammals, more than a dozen proteins that become prions have been identified, and a similar number has been found in fungi. In both mammals and fungi, variations in the prion conformation encipher the biological properties of distinct prion strains. Increasing evidence argues that prions cause many neurodegenerative diseases (NDs), including Alzheimer's, Parkinson's, Creutzfeldt-Jakob, and Lou Gehrig's diseases, as well as the tauopathies. The majority of NDs are sporadic, and 10% to 20% are inherited. The late onset of heritable NDs, like their sporadic counterparts, may reflect the stochastic nature of prion formation; the pathogenesis of such illnesses seems to require prion accumulation to exceed some critical threshold before neurological dysfunction manifests.
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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.