ReviewNeuron2016
Prions and Protein Assemblies that Convey Biological Information in Health and Disease.
Review in Neuron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 92 citations in OpenAlex.
- The vicious cycle: unraveling the interplay between α-synuclein, mitochondrial dysfunction, and neuroinflammation in Parkinson's disease.Journal of neurology · 2026Review
- Distinct Tau PET Dynamics in Early vs. Late Age-of-Onset Alzheimer's disease.medRxiv : the preprint server for health sciences · 2026Article
- β-Amyloid induces microglial expression of GPC4 and APOE leading to increased neuronal tau pathology and toxicity.Molecular neurodegeneration · 2025Article
- Linking dietary patterns to Alzheimer's disease biomarkers with network mathematical modeling could enable new approach methodologies in preventative AD research: a narrative interdisciplinary review.Frontiers in nutrition · 2025Review
- Tau in neurodegenerative diseases: molecular mechanisms, biomarkers, and therapeutic strategies.Translational neurodegeneration · 2024Review
- Site-selective peptide bond hydrolysis and ligation in water by short peptide-based assemblies.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- DnaJC7 specifically regulates tau seeding.eLife · 2023Article
- DnaJC7 specifically regulates tau seeding.bioRxiv : the preprint server for biology · 2023Article
- α-Synuclein conformers reveal link to clinical heterogeneity of α-synucleinopathies.Translational neurodegeneration · 2023Review
- Liquid Droplet Aging and Seeded Fibril Formation of the Cytotoxic Granule Associated RNA Binding Protein TIA1 Low Complexity Domain.Journal of the American Chemical Society · 2023Article
- Aβ and tau prions feature in the neuropathogenesis of Down syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Populations of Tau Conformers Drive Prion-like Strain Effects in Alzheimer's Disease and Related Dementias.Cells · 2022Review
- Default Mode Network quantitative diffusion and resting-state functional magnetic resonance imaging correlates in sporadic Creutzfeldt-Jakob disease.Human brain mapping · 2022Article
- Melatonin: Regulation of Prion Protein Phase Separation in Cancer Multidrug Resistance.Molecules (Basel, Switzerland) · 2022Review
- Distinct populations of highly potent TAU seed conformers in rapidly progressing Alzheimer's disease.Science translational medicine · 2022Article
- Assessment of Attentional Processes in Patients with Anxiety-Depressive Disorders Using Virtual Reality.Journal of personalized medicine · 2021Article
- Tau seeding in chronic traumatic encephalopathy parallels disease severity.Acta neuropathologica · 2021Article
- Anatomic survey of seeding in Alzheimer's disease brains reveals unexpected patterns.Acta neuropathologica communications · 2021Article
- Tau strains shape disease.Acta neuropathologica · 2021Review
- Hierarchical chemical determination of amyloid polymorphs in neurodegenerative disease.Nature chemical biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Prions derived from the prion protein (PrP) were first characterized as infectious agents that transmit pathology between individuals. However, the majority of cases of neurodegeneration caused by PrP prions occur sporadically. Proteins that self-assemble as cross-beta sheet amyloids are a defining pathological feature of infectious prion disorders and all major age-associated neurodegenerative diseases. In fact, multiple non-infectious proteins exhibit properties of template-driven self-assembly that are strikingly similar to PrP. Evidence suggests that like PrP, many proteins form aggregates that propagate between cells and convert cognate monomer into ordered assemblies. We now recognize that numerous proteins assemble into macromolecular complexes as part of normal physiology, some of which are self-amplifying. This review highlights similarities among infectious and non-infectious neurodegenerative diseases associated with prions, emphasizing the normal and pathogenic roles of higher-order protein assemblies. We propose that studies of the structural and cellular biology of pathological versus physiological aggregates will be mutually informative.
Indexed as
Identifiers
What Socratic 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 Socratic graph.